COLUMBIA  LIBRARIES  OFFSITE 

HEALTH  SCIENCES  STANDAR|D 


HX641 23472 
RC348  .  H44  1 907    Diagnosis  of  organic 


RECAP 


t- 


s: 


^  rK<.*^^jrjxmoom€K^.^i^^ 


Columbia  ®  nibersitp  \^  oi 

in  tfje  dtp  of  ^eto  gork 

COLLEGE  OF  PHYSICIANS 
AND  SURGEONS 


jFrom  tfje  Hibrarp  of 

3Br.  CJjrigtian  ^.  ^erter 

Honateb  bp 
1920 


Digitized  by  the  Internet  Archive 

in  2010  with  funding  from 

Open  Knowledge  Commons 


http://www.archive.org/details/diagnosisoforganOOhert 


DIAGNOSIS  OF  ORGANIC 
NERVOUS  DISEASES 


BY 


CHRISTIAN  A.  HERTER,  M.D. 

PROFESSOR   OF   PHARMACOLOGY    AND    THERAPEUTICS   AT   COLUMBIA   UNIVERSITY 
VISITING    PHYSICIAN    TO    THE    CITY    HOSPITAL 


REVISED  AND  ENLARGED  BY 

L  PIERCE  CLARK,  M.  D. 

VISITING   NEUROLOGIST   TO    THE    RANDALl's   ISLAND    HOSPITALS  AND   SCHOOLS 

CONSULTING   NEUROLOGIST   AT  THE   MANHATTAN   STATE    HOSPITAL,    N.  Y. 

CONSULTING   NEUROLOGIST   AT   THE  CRAIG   COLONY   FOR   EPILEPTICS 

SONYEA,  N.  Y.  ;  ASSISTANT  NEUROLOGIST  AT  VANDERBILT  CLINIC 

(COLUMBIA    college)    NEW   YORK 


WITH  109  ILLUSTRATIONS 


G.  P.  PUTNAM'S   SONS 
NEW    YORK    AND    LONDON 

^be  1knickert)oc??er  press 
1907 


Copyright,  1892 

BY 

CHRISTIAN  A.  HERTER 
Copyright,  1907 

BV 

CHRISTIAN  A.  HERTER 

For  Revised  Edition 


Ube  1Rnicl?crbocF?cr  prces,  IRew  Jljorft 


PREFACE   TO   THE   SECOND   EDITION. 

The  uninterrupted  demand  for  the  first  edition  of  this 
little  manual  as  a  guide  in  the  teaching  of  the  diagnosis 
of  nervous  diseases  has  led  me  to  believe  that  a  revised 
and  modernized  edition  would  prove  welcome.  As  my 
interest  in  medicine  has  gradually  become  concentrated 
on  other  fields  than  those  of  neurology,  it  has  seemed 
wise  to  entrust  the  work  of  revision  to  one  identified 
with  the  teaching  and  practice  of  neurology.  Dr.  L. 
Pierce  Clark,  who  has  undertaken  the  revision,  has  con- 
tributed much  that  is  new  to  the  edition  now  offered  to 
the  profession,  without,  however,  altering  or  extending 
the  scope  of  the  earlier  publication.  Dr.  Clark  has  re- 
written in  greater  part  the  chapter  on  the  anatomy  and 
physiology  of  the  nervous  system,  and  has  modernized 
the  section  dealing  with  the  symptomatology  of  nervous 
diseases.  The  chapter  on  the  examination  of  the  patient 
has  been  wholly  rewritten.  These  and  the  new  illustra- 
tions added  will  be  found,  it  is  believed,  to  contribute 
a  revision  that  is  thorough  without  being  destructive  of 
the  original  plan  of  the  book.  It  has  been  thought  de- 
sirable to  alter  the  title  of  the  volume  in  order  to  express 
more  plainly  its  preponderant  relation  to  organic  nervous 
diseases. 

C.  A.  Herter. 

New  York,  Jan.  1907. 


Ill 


PREFACE. 

This  volume  is  designed  to  ai.d  the  student  and  general 
practitioner  in  the  recognition  of  the  commoner  forms  of 
nervous  disease.  While  the  book  is  in  every  respect 
elementary  in  character,  it  is  believed  that  the  subject  of 
which  it  treats  is  presented  with  sufificient  detail  to  make 
it  serviceable. 

The  arrangement  that  has  been  followed  in  the  presen- 
tation of  facts  is  somewhat  unusual  and  requires  notice. 
In  the  chapter  on  the  structure  and  functions  of  the 
nervous  system  no  effort  has  been  made  to  give  a  sys- 
tematic outline  of  the  anatomy  of  the  brain  and  spinal 
cord.  Indeed,  little  else  has  been  attempted  than  the 
presentation  of  those  facts  regarding  the  motor  and  sen- 
sory paths  that  are  of  practical  importance  in  diagnosis. 

The  chapter  on  symptomatology  contains  a  description 
of  the  most  important  symptoms  of  nervous  disease,  and, 
in  most  cases,  the  chief  facts  regarding  their  diagnostic 
significance  and  pathology.  In  the  chapter  on  localiza- 
tion many  of  the  facts  given  under  symptomatology  have 
been  restated.  The  justification  of  this  repetition  is 
found  in  the  belief  that  it  is  very  desirable  to  emphasize 
the  more  important  relations  between  symptoms  and 
lesions  by  changing  the  point  of  view. 

In  the  fourth  chapter,  on  the  diagnosis  of  the  nature 
of  the  lesion,  an  attempt  is  made,  first,  to  give  the  main 
facts  (from  the  standpoint  of  diagnosis)  in  the  pathology 


vi  PREFACE. 

of  the  different  classes  of  lesions,  and,  secondly,  to  show 
the  manner  of  employing  the  indications  that  are  derived 
from  the  onset,  from  etiology,  and  from  the  position  of 
the  lesion.  In  discussing  the  indications  derived  from 
etiology  (causal  indications)  considerable  space  has  been 
devoted  to  the  enumeration  of  the  varieties  of  disease 
that  may  result  from  different  causes,  in  the  belief  that  a 
knowledge  of  these  facts  will  frequently  help  in  forming 
a  conclusion  as  to  the  nature  of  the  lesion. 

Next  follows  the  chapter  on  clinical  types,  in  which, 
while  the  types  are  necessarily  somewhat  rigidly  drawn, 
an  attempt  is  made  to  impress  the  fact  that  here,  as  in 
the  classification  of  all  natural  phenomena,  we  must  be 
prepared  to  recognize  numerous  variations  in  type  and 
transitional  forms. 

No  subject  is  more  important  or  more  difficult  to  treat 
satisfactorily  than  the  distinction  of  functional  and 
organic  disease.  An  endeavor  is  made,  in  the  sixth 
chapter,  to  present  the  chief  points  of  distinction  between 
different  forms  of  functional  disease  and  the  organic 
conditions  with  which  they  may  be  confounded.  It  was 
considered  advisable,  on  the  whole,  to  make  a  rather 
sharp  separation  between  the  traumatic  neurosis  and 
hysteria. 

The  propriety  of  including  in  a  work  of  so  elementary 
a  nature  a  short  chapter  on  the  examination  of  the 
patient  will  hardly  be  questioned. 

The  illustrations  of  diagnosis  which  are  given  in  the 
eighth  chapter  are  designed  to  aid  the  student  in  the 
application  of  the  methods  of  diagnosis  to  actual  cases 
of  disease. 

C.  A.  Herter. 

839  Madison  Avenuk, 
March  7,  1892. 


CONTENTS. 


System 


Chapter  I. — The  Structure  and  Functions  of  the 
Nervous  System 

Introductory  Remarks 
The  Brain       . 
The  Spinal  Cord    . 
The  Sympathetic  Nervous 
The  Motor  Tract  . 
The  Sensory  Tract 
Reflex  Paths 
The  Spinal  Nerves 
The  Cranial  Nerves 
The  Meninges  of  the  Brain  and  Cord 
The  Blood-Supply  of  the  Spinal  Cord  and  Brain 
Cranio-Cerebral  Topography.     Spinal  and  Spinal 
Cord  Topography 

Chapter  II. — The  Symptomatology  of  Nervous  Dis 
EASES  

1.  Mechanical  Injury  . 

2.  Loss  of  Blood-Supply,  Partial  or 

3.  Inflammation   .... 

4.  Wasting  of  Xerve  Elements  . 
Motor  Paralysis     .... 

Convulsions 

Tremor   ...... 

Fibrillation 

Rigidity 

Contracture  and  Contraction 

Catalepsy 

Athetosis  and  Athetoid  Movements 

vii 


Complete 


I 
10 

19 
27 

29 

38 
43 
44 

47 
74 

75 

80 

84 
85 

85 

86 

86 

87 

95 

103 

106 

108 

III 

113 

115 


Vlll 


CONTENTS 


Eyes  and  Head 


Associated  Movements 
Inco-ordination 
Conjugate  Deviation  of  the 
Strabismus 
Diplopia 
Nystagmus     . 
Ptosis      .... 
Pupillary  Symptoms    . 
-      -  Laryngeal  Symptoms  . 
Abnormal  Reflex  Action 
Sensory  Symptoms 
Headache       .        .    ,     .    ^ 
Olfactory  Symptom?.    . 
Visual  Symptoms 
Ophthalmoscopic  Changes 
Auditory  Symptoms     . 
Vertigo   .... 
Gustatory  Symptoms  . 
Trophic  Symptoms  ,     .    . 
Vaso-Motor  Symptorns 
Mental  Symptoms 
Disturbances  of  Speech 
General  Symptoms 

Chapter  III. — The  Diagnosis  of  the  Position  of  the 
Lesion — Localization  .... 

a.  Cortex  Cerebri     ..... 

b.  White  Substance  and  Centrum  Ovale 

c.  Corpus  Callosum      .... 

d.  Corpus  Striatum      .... 

e.  Optic  Thalamus        .... 

/.    Internal  Capsule      .... 

g.  External  Capsule  and  Claustrum 

h.  Corpora  Quadrigemina    .   ,     . 

i..  Crus  Cerebri      .        ...... 

y.    Pons  .        .        .......... 

k.  Medulla  Oblongata 

I..  Cerebellum 

Base  of  the  Brain  .... 


CONTENTS 


IX 


Spinal  Cord    . 
Nerve- Roots 
Cauda  Equina 
Peripheral  Xerves 
Chapter  IV. — The  Diagnosis  of  the  Nature  of  the 
Lesion 

Hyperaemia 

Anaemia 

Hemorrhage 

Softening 

Thrombosis  of  Sinuses 

Inflammation 

Meningitis 

Abscess  .         .         . 

Tumor 

Degeneration 

I.  The  Onset  of  the  Symptoms 

II.  The  Causal  Indications 

III.  The  Position  of  the  Morbid  Process 

Chapter  V. — The  Diagnosis  of  Clinical  Types 

Meningitis 

Lumbar  Puncture  in  the  Diagnosis  of  Meningitis 

Cerebral  Hemorrhage  . 

Acute  Cerebral  Softening     . 

Meningeal  Hemorrhage 

Sinus-Thrombosis 

Infantile  Cerebral  Paralysis 

Abscess  of  the  Brain    . 

Intracranial  Tumor 

Intracranial  Aneurism 

Nuclear  Ophthalmoplegia    . 

Multiple  of  Disseminated  Sclerosis 

Bulbar  Paralysis  .... 

General  Paralysis  of  the  Insane . 

Hydrocephalus      .... 

Spinal  Meningitis 

Intra-Spinal  Hemorrhage    . 

Myelitis 


253 
267 
268 

273 

274 

275 
276 
277 
281 
284 
285 
286 
293 

295 
301 

305 
306 

350 

352 

355 
360 

367 
371 
379 
3^4 
386 

394 
397 
403 
406 
411 
416 
419 
422 
426 
432 
435 


CONTENTS 


Spastic  Paraplegia 

Locomotor  Ataxia 

Ataxic  Paraplegia 

Friedreich's  Disease 

Progressive  Muscular  Atrophy 

The     Peroneal     Form     of     Progressive     Muscular 

Atrophy 

Pseudo-Hypertrophic  Paralysis 

Erb's  Type  of  Progressive  Muscular  Dystrophy 

Intra-Spinal  Tumor 

Syringomyelia 

Neuritis 

Diseases  of  Special  Nerves 

Tumors  of  Peripheral  Nerves  .... 
Lesions  of  the  Cauda  Equina  .... 
Multiple  Neuritis 

Chapter  VL — The  Distinction  of  Functional  and 
Organic  Disease 

Hysteria 

The  Traumatic  Neurosis  or  Psycho-Neurosis  . 

Neurasthenia 

Epilepsy 

Migraine 

Chorea 

Paralysis  Agitans 

Neuralgia 

Occupation  Neuroses 

Delirium  Tremens 

Cerebral  Concussion 

Malingering 

Chapter  VIL — The  Examination  of  the  Patient 

Chapter  VIIL — Illustrations  of  Diagnosis 

Index     


DIAGNOSIS    OF    ORGANIC 
NERVOUS    DISEASES 


DIAGNOSIS  OF  ORGANIC 
NERVOUS  DISEASES 


CHAPTER  I. 

THE    STRUCTURE    AND    FUNCTIONS    OF    THE    NERVOUS 

SYSTEM. 

Introductory  Remarks. — Simple  dissection  of  the 
cerebro-spinal  axis  in  the  fresh  state  reveals  little  beyond 
the  coarse  arrangement  of  the  gray  and  white  masses. 
But  in  specimens  that  have  been  prepared  by  careful 
maceration  in  alcohol  or  a  solution  of  bichromate  of 
potash,  it  is  possible  to  remove  with  a  forceps  bundle 
after  bundle  of  fibres  from  without  inward,  and  with 
such  nicety  that  the  general  course  and  relative  disposi- 
tion of  many  such  bundles  or  tracts  may  be  readily 
demonstrated.  Indeed,  in  the  hands  of  Meynert,  Bur- 
dach,  Foville,  and  others,  this  method  of  cleavage  or 
teasing  has  yielded  results  of  the  highest  importance. 
Still,  for  the  elucidation  of  the  more  minute  relations  of 
the  gray  matter  and  the  complicated  systems  of  fibres,  it 
is  not  wholly  adequate.  Nor  is  it  possible,  with  the 
microscope  and  modern  methods  of  staining  cells  and 
fibres,   to  determine  precisely  their  connections  or  to 


2  DISEASES   OF   THE   NERVOUS   SYSTEM. 

unravel  the  network  of  interlacing  fibres,  for  at  best 
only  the  structure  of  isolated  elements  is  revealed  by- 
such  means. 

Fortunately,  there  are  other  methods  of  research. 
Disease  in  man  and  physiological  experiment  in  the 
lower  animals  aid  us  in  the  investigation  and  differentia- 
tion of  the  more  intricate  and  finer  relations  of  gray 
matter  and  fibre  tracts,  and  of  the  latter  to  one  another. 
For  when  nerve-fibres  are  separated  from  their  nutritive 
centres  (the  ganglion-cells),  either  by  some  morbid  pro- 
cess, as  frequently  occurs  in  man,  or  by  actual  section 
of  a  nerve  in  a  lower  animal,  such  fibres  degenerate  in 
the  portion  cut  off  from  the  ganglion-cells  by  the  lesion, 
and  hence  definite  bundles  of  fibres  may  often  be  found 
altered  in  structure  throughout  their  whole  extent.  On 
dissection  the  degenerated  portion  becomes  visible  to  the 
naked  eye  by  its  change  of  color,  and  under  the  micro- 
scope the  altered  structure  of  the  fibres  is  very  marked. 
This  process  is  known  as  secondary  degeneration.  The 
descending  degeneration  of  the  motor  tract  in  the  brain 
and  in  the  lateral  and  anterior  columns  of  the  cord  fol- 
lowing coarse  lesions  in  the  cerebro-spinal  axis  is  an 
example  of  this  process,  the  fibres  of  the  motor  tract 
being  separated  from  their  nutritive  ganglion-cells  in  the 
cerebral  cortex. 

Again,  after  tearing  out  accessible  nerves  and  their 
end-organs,  such  as  the  optic  nerve  and  the  eye,  in  newly 
born  animals,  certain  groups  of  ganglion-cells  undergo  a 
sort  of  retardation  in  development  and  an  atrophy  from 
non-use;  and  when,  in  other  living  animals,  such  groups 
of  cells  are  experimentally  removed,  the  fibres  leading 
thence  to  the  end-organ  degenerate.  This  method  of 
investigation  is  known  as  Gudden's  atrophy  method. 
While  extremely  useful,  it  is  as  yet  rather  restricted  in 


THE  NERVOUS  SYSTEM.  3 

its  application,  since  the  lower  animals  only  can  be 
directly  experimented  upon,  and  the  facts  thus  ascer- 
tained cannot  always  be  properly  transferred  to  human 
physiological  anatomy. 

Still  another  method  of  great  value  is  one  developed 
by  Flechsig  and  originally  suggested  by  Meynert.  Cer- 
tain tracts  of  nerve-fibres  in  the  central  nervous  system 
have  been  found  to  develop  their  myeline  sheaths  at 
different  periods  of  time.  For  instance,  the  fibres  of  the 
posterior  nerve-roots  receive  their  myeline  sheaths  as 
early  as  the  seventh  month  of  foetal  life,  while  those  of 
the  motor  tract  do  not  become  perfected  until  after  birth. 
The  microscope  easily  differentiates  such  bundles,  and 
even  to  the  naked  eye  the  medullated  fibres,  by  their 
white  color,  contrast  strongly  in  transverse  section  with 
the  gray  non-medullated  fibres. 

The  functions  of  the  central  nervous  system  have  been 
studied  by  experimental  stimulation  and  destruction  of 
certain  portions  of  the  brain  and  cord  in  lower  animals, 
but  the  results  of  such  experiments  are  not  always  ap- 
plicable to  man.  Most  of  our  knowledge  of  cerebral  and 
spinal  localization  has  been  acquired  by  the  careful 
observation  of  the  symptoms  of  organic  lesions  in  man, 
and  their  comparison  with  the  pathological  conditions 
observed  at  autopsies. 

Investigations  in  the  realm  of  histology  have,  in  recent 
years,  added  much  to  our  knowledge  of  the  finer  nervous 
anatomy.  In  this  field  Golgi  and  Ramon  y  Cajal  have 
rendered  inestimable  service  and  have  made  possible  a 
fuller  conception  of  the  anatomical  structure  of  the  central 
nervous  system  embodied  in  the  neuron  theory  suggested 
by  Waldeyer.  This  theory  pictures  the  central  nervous 
system  as  composed  of  various  systems  of  units,  the  cell 
and  fibre  of  the  older  parlance  being  combined  in  the 


Nerve-cell 


,^    Dendrites 


■"  Nerve  process 
Collateral 


Medullary  sheath 


Axis-cylinder 


Neurilemna 


Terminal  ramification 

FIG.   I. 
Diagram  of  a  neuron.     (Stohr.) 


THE   NERVOUS   SYSTEM.  5 

neuron  of  the  new.  In  the  neuron  therefore  are  combined 
(a)  the  cell  body  containing  various  anatomical  struc- 
tures including  the  nucleus  and  nucleolus,  (b)  the  axis- 
cylinder  process  which  is  the  means  of  transmitting 
impulses  from  one  set  of  neurons  to  another  and  the  band 
by  which  the  neurons  are  chained  together  into  systems, 
and  (c)  the  dendrites  which  are  the  other  processes  from 
the  cell  body  whose  function  it  probably  is  to  perceive 
or  apprehend  impulses  and  carry  them  over  from  other 
neurons.  The  dendrites  thus  serve  for  the  reception  and 
diffusion  of  sensations  while  their  combination  and  ex- 
tension may  be  conceived  as  taking  place  in  the  cell 
body  and  their  ultimate  transmission  from  higher  to 
lower  groups  of  neurons  is  accomplished  through  the 
axis-cylinder  process. 

This  conception  of  the  nerve-cell  and  -fibre  as  consti- 
tuting a  single  organ,  the  neuron,  and  of  the  central 
nervous  system  as  being  made  up  of  groups  of  these 
organs  which  are  in  themselves  separate  and  distinct, 
has  not  met  with  entire  acceptance  and  corroboration, 
although  its  main  features  are  well  founded.  Bethe  and 
Apathy  claim  to  have  demonstrated  histologically  a  fibre 
continuity  between  two  separate  neurons,  which  they 
think  sufficiently  demonstrates  the  non-existence  of  the 
neuron  as  an  independent  unit;  while  Held  and  more 
recently  Nissl  have  put  forward  the  theory  of  the  great 
functional  importance  of  the  intercellular  substance  and 
have  observed  its  minute  fibrillary  structure.  Whether  or 
not  these  views  shall,  in  the  future,  be  proven  correct  is 
immaterial  for  the  present  purpose.  If  established  they 
may  be  accepted  as  corollaries  to  the  neuron  conception, 
while  its  principle  will  remain.  For  the  purposes  of  this 
book,  therefore,  we  shall  accept  the  conceptions  of  the 
neuron  theory. 


THE   NERVOUS   SYSTEM.  7 

shape  are  illustrated  herewith.  Many  qualifying  names 
have  been  applied  to  them,  such  as  angular,  granular, 
pyramidal,  ganglion,  multipolar,  globose,  round,  spindle- 
shaped,  etc.,  all  of  which  are  being  superseded  by  terms 
applying  more  directly  to  a  given  neuron  system.  The 
nerve-fibre  or  axis-cylinder  process  of  the  neuron  lacks 


FIG.   3. 

Diagram  to  illustrate  the  more  important  varieties  of  nerve-fibres.  A  and  B, 
medullated  nerve-fibres.  S,  sheath  of  Schwann.  The  myeline  sheath  lies  be- 
tween the  sheath  of  Schwann  and  the  axis-cylinder.  N,  nucleus  of  the  sheath 
of  Schwann.  IS,  incisures  of  Schmidt.  Node,  constriction  separating  two  seg- 
ments of  a  nerve-fibre.  C,  a  nerve-fibre  without  a  medullary  sheath.  D,  fibre  of 
Remak,  from  sympathetic. 


uniformity  of  structure.  It  occurs  either  as  a  naked 
axis-cylinder,  or  an  axis-cylinder  clothed  with  a  myeline 
sheath.  Some  of  these  forms  of  fibres  are  figured  above, 
and  the  highest  form  of  fibre  is  shown  with  its  sheath  of 


8 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


Schwann,  myeline  sheath,  axis-cylinder,  Ranvier's  nodes, 
and  Schmidt's  incisions  (Fig.  3). 

For  the  purposes  of  support  and  protection  of  the 


'■'•st^- 


FIG.  4. 
Normal  Betz  cell  from  the  human  paracentral  lobule.     (Meyer.) 

neurons  of  varying  types  and  their  delicate  appendages, 
there  exists  a  tissue  known  as  the  neuroglia  which  is 
composed  of  branching  cells   and  fibres   derived  from 


THE   NERVOUS    SYSTEM.  9 

these  cells,  whose  function  is  probably  a  purely  supportive 
one  (see  Fig  2).  In  addition  to  these  there  are  other 
non-branching  cells  existing  chiefly  in  the  cerebral  cortex 
and  whose  function  is  probably  that  of  a  support  to  the 
more  delicate  nervous  structures. 

Besides  originating  and  receiving  nervous  impulses  the 
neuron  exercises  a  nutritional  influence  over  every  por- 
tion of  its  structure.  In  consequence  of  this,  when  an 
axis-cylinder  process  or  a  dendrite  is  severed  from  the 
body  of  the  neuron,  the  distal  portion  degenerates.  It 
will  be  perceived,  therefore,  that  the  direction  of  degen- 
eration in  a  nerve-fibre  does  not  necessarily  follow  the 
course  and  direction  of  the  impulse. 

There  is  also  in  the  course  of  time  some  trophic  dis- 
turbance in  the  cell  itself,  and  the  portion  of  the  fibre 
still  connected  with  it,  especially  in  very  young  animals. 
This  trophic  change  is  allied  histologically  to  secondary 
degeneration,  but  is  not  precisely  the  same  process.  It 
is  a  species  of  dystrophy  from  non-use,  and  partakes  also 
of  the  nature  of  arrest  of  development  when  it  occurs  in 
young  animals. 

Groups  of  neurons  of  the  larger  type,  such  as  are 
shown  in  Fig.  4,  may  be  considered  as  subsetving  a 
motor  function  wherever  met  with.  The  figure  repre- 
sents one  of  the  so-called  Betz  cells  found  in  and  char- 
acteristic of  certain  portions  of  the  motor  cortex,  but 
similar  neurons  occur  in  the  anterior  horns  of  the  spinal 
cord,  here  constituting  the  lower  or  second  set  of  neurons 
in  the  motor  system.  Groups  of  neurons  such,  for  ex- 
ample, as  those  above  designated  are  commonly  called 
''centres."  This  term  is  employed  correctly  only  in  a 
physiological  sense.  We  mean  thereby  any  group  of 
neurons,  not  necessarily  possessing  well-defined  topo- 
graphical limits,   which  act   conjointly   in   a  functional 


lO  DISEASES   OF   THE   NERVOUS   SYSTEM. 

capacity.  Sometimes  such  groups  are  widely  separated, 
although  functionally  associated.  They  are  therefore 
regarded  as  constituting  a  functional  centre. 

There  is  nothing  in  the  anatomical  features  of  nerve- 
fibres  to  give  us  a  clue  to  the  nature  of  their  functional 
activity.  Their  axis-cylinders,  apparently  insulated  by 
myeline  sheaths,  seem  to  be  conductors  of  nerve  force. 
The  axis-cylinders  vary  in  size,  but  the  significance  of 
such  variation  has  not  been  satisfactorily  explained. 
Many  of  the  largest  certainly  belong  to  fibre  systems  of 
great  length,  but  we  are  not  yet  warranted  in  assuming 
any  definite  relation  of  the  breadth  to  the  length  of 
these  elements. 

The  body  of  the  neuron  and  its  axis-cylinder  process 
contribute  respectively  the  gray  and  white  matter  of  the 
cerebro-spinal  axis.  The  gray  matter  completely  en- 
velops the  hemispheres  of  the  brain,  forming  a  layer 
known  as  the  cortex,  the  seat  of  the  higher  mental  func- 
tions. There  are  also  large  masses  of  gray  matter  at  the 
base  of  the  brain  in  the  basal  ganglia,  and  the  nuclear 
cells  of  the  cranial  nerves  are  scattered  through  the  in- 
terior of  the  crura,  pons,  and  medulla.  In  the  cerebel- 
lum the  gray  matter  has  a  very  complex  arrangement, 
while  in  the  cord,  on  transverse  section,  it  is  seen  to 
have  an  H-like  contour  as  it  lies  imbedded  in  the  midst 
of  columns  of  white  fibres. 

The  Brain. — The  accompanying  illustrations  offer  a 
readier  means  of  acquiring  a  knowledge  of  the  topo- 
graphical distribution  of  the  chief  convolutions  and 
fissures  of  the  cerebrum  than  would  a  description  in  the 
text.  The  cortex  varies  in  depth  and  structure  in  differ- 
ent regions,  so  that  no  less  than  eight  distinct  types  of 
cortical  lamination  have  been  noted  by  some  investiga- 
tor«      For  instance,  in  some  regions  there  are  but  three 


THE   NERVOUS   SYSTEM. 


II 


layers  in  the  cortex,  in  others  seven.  The  neurons  vary 
greatly  in  type  and  size  in  the  various  layers  and  re- 
gions of  the  cortex.  The  largest  are  found  in  the  motor 
convolutions. 

These  differences  of  structure  subserve  differences  in 
function,  and  modern  research  has  localized,  more  or  less 
perfectly,  areas  for  voluntary  motion,  speech,  cutaneous 


FIG.   5. 

Diagram  showing  the  division  of  the  brain  into  lobes,  outer  surface,  and  of 
right  hemisphere. 

sensation,  visual,  auditory,  and  olfactory  impressions, 
and  has  outlined  with  some  degree  of  certainty  regions 
which  subserve  the  higher  intellectual  operations.  The 
accompanying  diagrams  indicate  with  sufficient  clearness 
the  relative  positions  of  these  regions. 

It  is  well  to  bear  in  mind  that  besides  the  fibres  passing 
out  from  these  cortical  areas  to  the  periphery  of  the 
body,  there  are  numerous  bundles  of  fibres  which  con- 
nect with  one  another  different  lobes  and  different  con- 
volutions^ and  join  certain  parts  of  the  cortex  with  certain 


12 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


FIG.  6. 

Diagram  of  the  inner  or  medial  surface  of  the  brain  showing  the  division  into 
lobes.  The  parietal  lobe  does  not  extend  so  near  the  corpus  callosum  as  here 
indicated. 


Par  I  eto 
bccipita 


FIG.  7. 

Diagram  showing  the  chief  convolutions  and  fissures  on  the  outer  surface  of  the 
right  hemisphere. 


THE   NERVOUS   SYSTEM. 


13 


of  the  basal  ganglia  and  the  cerebellum.  The  former 
fibres,  which  in  a  manner  project  the  organism  upon  the 
cortex,  as  the  world  is  projected  upon  a  map,  are  often 
termed  "projection"  fibres;  while  most  of  the  latter, 
which  undoubtedly  serve  to  bring  various  parts  of  the 
brain  into  conjoint  and  harmonious  action^  are  known  as 
"association"  fibres  (see  Fig  15). 

The  two  cerebral  hemispheres  are  associated  in  func- 


FIG.   8. 

Diagram  showing  the  chief  convolutions  and  fissures  on  the  inner  or  medial 
surface  of  the  right  hemisphere.    . 


tion  by  the  large  bundles  of  fibres  passing  from  the 
cortex  of  one  side  to  that  of  the  other,  and  constituting 
the  corpus  callosum.  In  addition  to  this  great  commis- 
sure there  are  three  small  ribands,  known  as  the  anterior, 
middle,  and  posterior  commissures,  in  the  third  ven- 
tricle, which  are  to  a  certain  extent  bonds  of  union 
between  the  two  halves  of  the  brain.  Of  these  commis- 
sures, the  anterior  is  the  most  important,  and  is  largely 
connected  with  the  olfactory  system,  while  the  middle  is 
of  little  or  no  importance. 


14 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


FIG. 


FIG.   lO. 


Diagram  showing  the  position  of  the 
cortical  motor  area  on  the  outer  sur- 
face of  the  hemisphere.  The  vertical 
shading  represents  the  position  of  the 
leg  centre.  The  horizontal  shading 
shows  the  position  of  the  face  centre. 
The  dotted  area  shows  the  position  of 
the  arm  centre. 


Diagram  showing  the  position  of  the 
leg  centre  on  the  inner  surface  of  the 
right  hemisphere.  R  indicates  the 
position  of  the  fissure  of  Rolando  on 
the  outer  surface. 


Ol  tacto 


VltWAk    CtHTtn 


FIG,  II. 


FIG.   12. 


Diagram  showing  the  cortical  visual 
centres  on  the  outer  surface  of  the 
right  hemisphere.  The  horizontal  lines 
show  the  approximate  position  of  the 
half-vision  centre.  The  dotted  areas 
show  the  position  of  the  supposed 
higher  visual  centre. 


Diagram  showing  the  position  of  the 
visual  (half-vision)  centre  and  the 
probable  position  of  the  olfactory  cen- 
tre on  the  inner  surface  of  the  right 
hemisphere. 


FIG.  13. 

Diagram  showing  the  position  of  the 
auditory  centre  in  the  first  temporal 
convolution. 


FIG.  14. 

Diagram  showing  the  position  of  the 
motor  speech  centre  in  the  left  hemi- 
sphere. 


THE   NERVOUS   SYSTEM. 


15 


Very  little  is  known  concerning  the  functions  of  the 
caudate  nuclei.  The  lenticular  nucleus  and  the  optic 
thalamus  are  of  great  importance  as  primary  terminals 
of  the  great  sensory  systems  from  the  periphery.  The 
optic  thalamus  is  of  especial  importance  in  this  particu- 
lar.    Moreover,  this  mass  forms  a  primary  termination 


FIG.  15. 

The  association  fibres.  A,  between  adjacent  convolutions  ;  B,  between 
frontal  and  occipital  areas  ;  C,  between  frontal  and  temporal  areas,  cin^- 
lum ;  D,  between  frontal  and  temporal  areas,  fasciculus  uncinatus ;  E, 
between  occipital  and  temporal  areas,  fasciculus  longitudinalis  inferior  ; 
C  N,  caudate  nucleus ;  O  T,  optic  thalamus.     (Starr.) 

for  ocular  and  auditory  fibres  from  the  periphery  and  is 
connected  with  the  visual  and  auditory  areas  of  the 
cerebral  cortex.  It  may,  therefore,  be  regarded  as  the 
great  way  station  for  the  entire  sensory  system.  The 
anterior  bodies  of  the  corpora  quadrigemina  are  asso- 
ciated with  the  function  of  sight,  while  the  posterior 
are  associated  with  the  function  of  hearing.  These 
bodies  also  have  other  functions  not  well  known. 

All  the  fibres  connecting  the  periphery  with  the  brain 
hemispheres  pass  through  the  crura  cerebri  (the  olfactory 


i6 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


and  optic  tracts  excepted).    There  are  in  addition  special 
bundles  of  fibres  connecting  the  cerebrum  and  cerebel- 


FIG.  i6. 


The  projection  tracts  joining  the  cortex  with  lower  nerve  centres.  Sagittal  sec- 
tion showing  the  arrangements  of  tracts  in  the  internal  capsule.  A,  tract  from 
the  frontal  lobe  to  the  anterior  half  of  the  capsule,  thence  in  part  to  the  optic 
thalamus,  A^,  and  in  part  to  the  pons,  and  thus  to  the  cerebellar  hemisphere  of  the 
opposite  side;  B,  motor  tract  from  the  central  convolutions  to  the  facial  nucleus 
in  the  pons  and  to  the  spinal  cord  ;  C,  sensory  tract  from  posterior  columns  of  the 
cord,  through  the  posterior  part  of  the  medulla,  pons,  crus,  and  capsule  to  the  pari- 
etal lobe;  D,  visual  tract  from  the  optic  thalamus  (O  T)  to  the  occipital  lobe;  E, 
auditory  tract  from  the  int.  geniculate  body  (to  which  a  tract  passes  from  the 
VIII.  n.  nucleus)  to  the  temporal  lobe;  F,  superior  cerebellar  peduncle;  G,  mid- 
dle cerebellar  peduncle;  H,  inferior  cerebellar  peduncle;  C  N.  caudate  nucleus; 
C  Q,  corpora  quadrigemina.     The  numerals  refer  to  the  cranial  nerves.     (Starr.) 

lum,  the  fronto-,  occipito-,  and  temporo-pontine  tracts, 
which   ultimately   terminate  in   the  cortex  of  the  great 


THE   NERVOUS   SYSTEM. 


17 


lobes  of  the  cerebellumby  means  of  ponto-cerebellar  fibres 
which  pass  out  through  the  middle  cerebellar  peduncles. 

In  a  transverse  section  through  the  crura  the  various 
tracts  and  nuclei  lie  as  shown  in  diagram  19.      The  third 
nerve  nucleus  lies  in  the  floor  of  the  aqueduct  of  Sylvius, 
and  the  fibres  of  the  nerve 
pass  out  through  the  crus 
on  their  way  to  the  orbit. 

The  practical  and  use- 
ful facts  in  the  anatomy 
of  the  pons  and  medulla 
relate  especially  to  the 
disposition  of  the  cranial 
nerve-nuclei  and  certain 
bundles  of  fibres.  The 
superficial  origin  of  the 
cranial  nerves  is  seen  in 
Fig.  17.  A  knowledge  of 
the  relative  positions  of 
their  nuclei  is  best  gath- 
ered from  the  accompany- 
ing diagrams  (18  and  19). 

The  relations  of  certain 
of  the   cranial  nerves  to 
the   motor   tract   will  be 
treated  of  in  connection    "•^'"^es. 
with  the  description  of  the  latter. 

The  superficial  anatomy  of  the  cerebellum  is  portrayed 
in  the  two  accompanying  illustrations  (Figs.  20,  21)  of  its 
dorsal  and  ventral  aspects.  Each  hemisphere  of  the 
cerebellum  is  joined  to  the  mid-brain,  to  the  pons,  and  to 
the  medulla  by  three  large  diverging  bundles  of  fibres, 
known  respectively  as  the  superior,  middle,  and  inferior 
cerebellar  peduncles.  The  peduncles  are  shown  in  Fig.  22. 


FIG.  17, 
The  base  of  the  brain  and  the  cranial 


i8 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


We  are  still  greatly  in  the  dark  as  regards  the  physiol- 
ogy of  the  cerebellum.  Disease  here  so  easily  produces 
indirect  effects  upon  the  pons  and  medulla  that  the 
actual  focal  symptoms  are  often  obscured.  But  there  is 
undoubted  evidence  of  the  relation  of  the  organ  to  bodily 
equilibrium,  for  disease  in  a  peduncle  may  produce 
forced  movements  to  one  side  or  the  other,  and  the  inco- 
ordination known  as  cerebellar  staggering  or  titubation 


CORP.   QUAD. 


"^""SSAT, 


FIG.  l8. 

Diagram  showing  the  nuclear  origin  of  the  cranial  nerves ;  the  medulla,  pons, 
and  crus  being  seen  from  the  side,  and  represented  as  transparent.  The  sensory 
structures  are  in  red.  Ill,  oculo-motor  nucleus — i,  fibres  from  the  cells  that  sub- 
serve accommodation  ;  2,  fibres  from  cells  subserving  the  reflex  action  of  the  iris; 
3,  fibres  from  cells  innervating  the  external  muscles  of  the  eye.  P.  L.  B.,  poste- 
rior longitudinal  bundle  associating  certain  cells  of  the  Illd  nucleus  with  cells 
of  the  Vlth  nucleus.  The  portion  of  this  bundle  which  lies  between  the  Vlth 
nucleus  and  the  cord  is  not  represented.  Vm,  motor  nucleus  of  trigeminus.  Vs, 
sensory  nucleus.  The  ascending  sensory  root  of  the  5th  is  reprinted  as  coming 
from  the  substantia  gelatinosa  of  the  cord.  The  descending  or  trophic  root 
arises  in  the  quadrigeminal  region.  VII,  facial  nucleus.  VIII,  auditory  nuclei. 
IX,  glosso-pharyngeal  nucleus.  X,  vagus  nucleus.  The  roots  of  the  vagus  receive 
filaments  from  the  nucleus  ambiguus.  XI,  spinal  accessory  nucleus.  XII,  hypo- 
glossal nucleus. 


is  due  to  disturbance  of  the  middle  portion  of  the  cere- 
bellum, the  vermis,  or  worm.  There  is  some  evidence 
that  it  influences  the  power  of  muscular  movements,  and 
there  is  also  some  probability  that  this  organ  forms  a  sub- 
stratum for  some  of  the  intellectual  processes,  through 
its  intimate  connection  with  the  frontal  lobes  of  the  cere- 
brum by  means  of  the  fronto-cerebellar  tract  of  fibres 


THE   NERVOUS   SYSTEM. 


19 


SUP. 


PONS 


INf. 


(sometimes    called    "intellectual  tract").      {Vide   Fig. 
22.) 

For  further  information  as  to  the  disposition  of  the 
various  parts  of  the  brain,  the  reader  is  referred  to  works 
on  the  descriptive  anat- 
omy of  the  brain. 

The  Spinal  Cord. — 
The  spinal  cord  averages 
from  seventeen  to  eigh- 
teen inches  in  length,  and 
extends  from  the  superior 
plane  of  the  atlas  to  the 
second  lumbar  vertebra. 
The  spinal  canal  is  some 
nine  or  ten  inches  longer 
than  the  cord,  reaching  as 
it  does  through  the  re- 
maining lumbar  vertebras 
and  sacrum  to  the  coccyx. 
The  segments  of  the  cord 
are  short,  and  each  pair 
of  spinal  nerves  takes  a 
downward  direction  from 
the  segment  before  it 
reaches  the  intervertebral 
foramen.  The  intraspinal 
course  of  the  nerves  is 
longer  the  lower  we  de- 
scend the  cord,  so  that  the 
lumbar  and  sacral  pairs 
form  the  large  bundle  of  nerves  known  as  the  cauda 
equina  (horse-tail)  occupying  the  lower  end  of  the  spinal 
canal.  The  cord  is  not  of  uniform  diameter,  for  there  is 
an  intumescence  in  the  cervical  cord,  called  the  cervical 


Diagram  showing  the  nuclear  origin  of 
the  cranial  nerves  (except  the  auditorv). 
The  sensory  structures  are  in  red  and  the 
motor  in  black.  The  floor  of  the  4th  ven- 
tricle is  seen  from  above,  and  on  the  right 
side  the  structures  are  represented  as 
transparent.  VII,  the  facial  nucleus.  The 
fibres  from  this  nucleus  wind  round  the 
nucleus  of  the  abducens  nerve  (VI),  and 
make  their  exit  just  below  the  pons  IX 
and  X,  common  nucleus  of  the  glosso- 
pharyngeal and  vagus  nerves.  The  roots 
of  the  vagus  receive  filaments  from  the 
nucleus  ambiguus.  XI,  spinal  accessory 
nucleus.  XII,  hypoglossal  nerve.  V.  the 
trigeminus  nerve.  Fibres  pass  to  this 
nerve  from  above  (descending  or  trophic 
root),  from  below  (ascending  sensory  root), 
from  the  level  of  its  exit  from  a  sensory- 
nucleus,  and  from  a  motor  nucleus. 
P.L.B.,  posterior  longitudinal  bundle  con- 
necting the  Vlth  nucleus  below  with  the 
Illd  nucleus  above.  VIII,  the  striae 
acoustics. 


20  DISEASES   OF   THE   NERVOUS   SYSTEM. 


FIG.   20. 

Diagram  of  dorsal  surface  of  cerebellum,  showing  the  position  of   the  worm, 
[After  Edinger.) 


rA\0Oue 


FIG.    21. 
Diagram  of  ventral  surface  of  cerebellum.     (After  Edinger.) 


THE   NERVOUS    SYSTEM. 


21 


Sup  Pttt. 


enlargement,  due  to  the  fact  that  it  is  the  motor  and 
sensory  cord  centre  for  the  upper  extremities;  and  the 
lower  extremity  of  the  cord  also  presents  an  intumescence 
known  as  the  lumbar  enlargement,  containing  the  centres 
subserving  motion  and  sensation  in  the  lower  extremities, 
together  with  the  sexual,  anal,  and  vesical  centres.  The 
term  lumbar  enlargement  is  a  little  misleading,  and  it 
must  be  rem.embered  that  though  this  enlargement  gives 
rise  to  lumbar  nerves,  the 
greater  portion  of  it  is  con- 
tained in  the  lowest  part  of 
the  dorsal  region  of  the 
spine. 

The  spinal  cord,  taken 
as  a  whole,  must  be  studied 
from  two  points  of  view; 
first,  as  a  kind  of  cable 
through  which  nerve-im- 
pulses are  transmitted  to 
and  fro  between  the  periph- 
eral portions  of  the  body 
and  the  brain;  secondly,  as 
a  series  of  segments  super- 
imposed like  blocks  one  upon  the  other,  each  giving  rise 
to  a  pair  of  spinal  nerves,  and  each  serving  as  a  centre 
for  various  reflexes,  for  trophic  influences,  and  for  vas- 
cular control.  The  long  fibres  necessary  for  the  first 
purpose  are  disposed  in  columns  running  the  whole  length 
of  the  cord  and  surrounding  the  central  gray  matter. 

The  H-shaped  central  gray  matter  consists  of  the 
anterior  and  posterior  horns,  which  are  connected  with 
the  anterior  and  posterior  roots  of  the  spinal  nerves. 
The  lateral  and  anterior  columns  contain  the  motor-fibres 
from   the   cortex,    and    the   posterior    columns    certain 


Diagram  showing  the  three  peduncles 
of  the  cerebellum — the  superior  pedun- 
cle going  to  the  quadrigeminal  region, 
the  middle  peduncle  going  to  the  pons, 
and  the  inferior  peduncle  coming  from 
the  cord  below,     (After  Edinger.) 


22 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


sensory  tracts.  The  anterior  columns  are  often  called  the 
columns  of  Tiirck;  the  posterior  are  composed  of  the 
columns  of  GoU  and  Burdach.  Their  exact  positions 
are  indicated  in  the  accompanying  diagram  of  a  trans- 
verse section  of  the  cord. 

Reflex,  trophic,  and  vaso-motor  centres  are  situated 


ioo«s 


FIG.  23. 

Diagram  of  a  section  of  the  spinal  cord  in  the  cervical  region.  A.  C,  anterior 
commissure;  P.  C,  posterior  commissure;  I.  g.  s.,  intermediate  gray  substance  ; 
P.  Cor.,  posterior  cornu  ;  c.  c  p.,  caput  cornu  posterioris ;  1.  1.  1.,  lateral  limiting 
layer;  a.-l.  a.  t..  antero-lateral  ascending  tract,  which  extends  along  the  periphery 
of  the  cord.     (Gowers.) 


in  the  gray  matter.  The  various  reflexes  will  be  con- 
sidered elsewhere.  The  trophic  centres  in  the  anterior 
horns  regulate  the  nutrition  of  the  motor  nerves  and 
muscles,  and  the  destruction  of  them  is  followed  by  de- 
generation of  the  motor  nerves  and  atrophy  of  the 
muscles  innervated  by  them.     The  ganglia  of  the  pos- 


THE  NERVOUS   SYSTEM. 


23 


terior  roots  are  trophic  centres  for  most  of  the  fibres  of 
the  sensory  nerves,  but  a  few  of  the  posterior  root-fibres 
have  trophic  centres  in  the  posterior  horns.  There 
are  trophic  centres,  also,  for  viscera,  bones,  joints, 
and  for  the  skin  and  nails,  all  along  the  cord,  and 
these  are  probably  situated  in  the  gray  matter  about  the 
central  canal.  There  are  communicating  nerve-filaments 
between  them  and  the  ganglia  and  fibres  of  the  sympa- 
thetic nervous  system. 

It  must  be  borne  in  mind  that  the  spinal  cord,  like  the 
brain,  is  composed  of  two  symmetrical  halves,  but  more 
closely  bound  together.  Throughout  its  whole  extent 
fibres  pass  from  one  side  to  the  other.  There  are,  first, 
the  sensory  nerve-fibres,  which  decussate  along  the  whole 
of  the  cord,  and  besides  these  there  are  commissural 
fibres  between  the  anterior  columns  and  anterior  horns. 

The  following  is  a  table,  slightly  modified  in  the  light 
of  recent  investigations  from  the  excellent  one  first 
elaborated  by  Starr,  which  shows  the  relation  between 
each  segment  of  the  spinal  cord  and  the  principal  muscles 
or  groups  of  muscles,  sensory  areas,  and  reflexes  in 
connection  with  it. 


Segment  0/ 
cord 

Nerves 

Muscles 

Sensory  areas 

Reflexes 

Second  and 
third 
cervical 

Occipitalis    ma- 
jor and  minor 

Auricularismag. 

Superficialis 
colli 

Supraclavicular 

Sterno-mastoid 
Trapezius 
Scaleni    and  neck 
muscles 
Diaphragm 

Neck  and  back 
of  head 

Hypochon- 

drium  (?) 

Fourth 
cervical 

Supraclavicular 
Circumflex 
Musculo-cuta- 
neous 
Musculo-spiral 

Diaphragm 
Supra-  and  infra- 
spinatus 
Deltoid 

Supinator  longus 
Rhomboidei 

Neck 

Superior  surface 

of  shoulder 
Outer  surface  of 

arm 

Cilio  -  spinal 
(^4th  cer\'ic'l 
to    2d    dor- 
sal) 

24 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


Segment  of 
cord 

Nerves 

Muscles 

Sensory  areas 

Reflexes 

Fifth 

Supraclav 

cular 

Deltoid 

Back   of   shoul- 

Scapular 

cervical 

Circumfl 

ex 

Biceps  and 

der  and  arm 

(5th  cervic'l 

External 

cuta- 

coraco-brachialis 

Outer     side     of 

to   1st  dor- 

neous 

Supinator    longus 

arm  and    fore- 

sal) 

Internal 

cuta- 

and  brevis 

arm 

Biceps  jerk 

neous 

Rhomboidei 

Supinator 

Posterior 

spinal 

Deep   muscles    of 

jerk 

branches 

shoulder-blade 
Pectoralis  (clavic- 
ular part) 
Teres  minor 
Serratus  magnus 
Brachialis  anticus 

Sixth 

External 

and 

Biceps 

Outer  side   and 

Elbow    jerk 

cervical 

internal 

cuta- 

Brachialis  ant. 

front    of    fore- 

(triceps) 

neous 

Pectoralis  (clavic. 

arm. 

Wrist  jerk 

Radial 

part) 
Subscapular 
Serratus  mag. 
Triceps 
Extensors  of 

wrist  and  fingers 
Pronators 

Back    of     hand 
(radial     distri- 
bution) 

Seventh 

External 

and 

Triceps     (long 

Radial  and  me- 

Palmar 

cervical 

internal 

cuta- 

head) 

dian     distribu- 

(7th   cervi- 

neous 

Extensors  of 

tion 

cal    to    1st 

, 

Radial 

wrist  and  fingers 

dorsal) 

Median 

Pronators 

Posterior 

spinal 

Flexors  of  wrist 

branches 

Subscapular 
Pectoralis    (costal 

part) 
Serratus  mag. 
Latissimus  dorsi 
Teres  major 

Eighth 

Internal 

cuta- 

Triceps(long  head) 

Inner     side     of 

cervical 

neous 

Flexors    of    wrist 

arm    and  fore- 

Ulnar 

and  fingers 
Small    muscles  of 
hand 

arm 
Ulnar    area     of 
hand 

First  dorsal 

Int.     cutaneous 

Extensors  of 

Inner     side     of 

nerve  of 

Wris- 

thumb 

arm    and   fore- 

berg 

Small  muscles    of 

hand 
Thenar  and  hypo- 

thenar  muscles 

arm 

THE   NERVOUS   SYSTEM. 


25 


Segment  of 
cord 

Nerves 

Muscles 

Sensory  areas 

Reflexes 

Second 

Intercosto- 

Inner     side     of 

dorsal 

humeral 

arm  near  axilla 

Second  to 

Intercostals  and 

Muscles    of    back 

Skin  of  back  and 

Epigastric 

twelfth 

dorsal  posterior 

and  abdomen 

upper     gluteal 

(4th  to  7th 

dorsal 

nerves 

Erectores  spinae 

region,   and  of 
breast  and  ab- 
domen in  bands 

dorsal) 
Abdominal 
(7th  to  nth 

running  down- 
ward &  forward 
Skin   over  groin 

dorsal) 

First 

Ilio-hypogastric 

Ilio-psoas 

Cremasteric 

lumbar 

Ilio-inguinal 

Sartorius 

and     front     of 

(ist    to    3d 

Rectus 

scrotum 
Outer  surface  of 

lumbar) 

Second 

Genito-crural 

Ilio-psoas 

lumbar 

External  cuta- 
neous 

Sartorius 
Quadriceps  fem'ris 

Quadriceps  fem'ris 

thigh 

Third 

Anterior 

Anterior  surface 

Knee-jerk 

lumbar 

Crural 

Internal      cuta- 
neous 
Long  saphenous 

Anterior    part    of 

biceps 
Inner   rotators    of 

thigh 

of  thigh 

Obturator 
Internal      cuta- 

Adductors of  thigh 

Adductors  of  thigh 
Abductors  of  thigh 

Inner     side     of 

Fourth 

Gluteal  (4th 

lumbar 

neous 

thigh,  leg,  and 

to  5th  lum- 

Long saphenous 

Flexors  of  knee 

foot 

bar) 

Obturator 

Tibialis  anticus 

External   popli- 

Peroneuslongus 

Fifth 

Outward    rotators 

Outer  and  back 

Ankle  clonus 

lumbar 

teal 

of  thigh 

side  of  leg  and 

External  saphe- 

Flexors of  knee 

foot 

nous        [neous 

Flexors  of  ankle 

Sole  of  foot 

Musculo-cuta- 

Extensors  of  toes 

Plantar 

Same      as      5th 

Peronei 

First  and 

Flexors    and     ex- 

Same     as      5  th 

Plantar  (5th 

second 

lumbar 

tensors  of  ankle 

lumbar 

lumbar     to 

sacral 

Small  sciatic 

Long  flexor  of  toes 
Small  foot  muscles 

2d  sacral) 

Third, 

Perineal 

Back   of   thigh. 

Vesical    and 

fourth, 

Pudic 

Muscles   of    blad- 

anus,perineum, 

anal  centres 

and  fifth 

Inferior  hemor- 

der, rectum,  and 

genital  organs 

sacral 

rhoidal 

Inferior  puden- 
dal 
Coccygeal 

external   genitals 

Fifth  sacral 

Coccygeus 

Skin  about  anus 

&  coccygeal 

1 

and  coccyx 

26  DISEASES   OF   THE   NERVOUS   SYSTEM. 

In  addition  to  the  reflex  centres  indicated  in  the  table, 
and  which  have  great  practical  importance,  there  are 
others  whose  precise  location  has  not  yet  been  determined 
(such  as  the  parturition  centre  and  the  erectile  and  ejac- 
ulatory  centres),  although  we  know  they  are  in  the  lumbar 
enlargement. 

The  reflexes  here  given  vary  somewhat  in  importance. 
The  knee  jerk  and  the  character  of  the  plantar  response 
are  of  greatest  importance.  The  latter  is  known  as  the 
Babinski  sign  and  will  be  further  dealt  with  in  the  chap- 
ter on  diagnosis. 

It  is  always  to  be  borne  in  mind  that  changes  in  the 
character  of  a  given  reflex  mean  primarily  the  involve- 
ment of  the  cord  segment  in  which  it  is  represented.  For 
example,  in  spinal-cord  tumor  we  shall  have  an  absence 
of  or  a  change  in  the  character  of  all  the  reflexes,  super- 
ficial and  deep,  up  to  the  segment  involved. 

The  sympathetic  nervous  system  was  originally  so 
called  because  of  its  supposed  relationship  to  emotional 
states.  The  name  is  obviously  bad  and  should  be 
dropped,  more  especially  since  this  system  subserves  no 
such  purpose.  It  is  composed  of  the  afferent  and  effer- 
ent nerve-fibres  distributed  to  the  various  viscera  and 
the  vascular  apparatus,  the  ultimate  centres  for  which 
are  within  the  cerebro-spinal  axis.  The  so-called  sym- 
pathetic system  pet-  se  consists  of  a  series  of  ganglia 
lying  above,  between  the  cranial  and  facial  bones,  and 
running  down  each  side  of  the  vertebral  column  from 
the  skull  to  the  coccyx,  connected  together  by  non- 
medullated  nerve-fibres,  sending  branches  to  the  smaller 
terminal  ganglia  of  the  tissues  or  viscera,  and  having 
communications  with  most  of  the  cranial  and  spinal 
nerves,  and  through  them  with  the  central  nervous  sys- 
tem (see  Fig.  24).     Besides  the  pairs  of  lateral  ganglia 


THE   NERVOUS   SYSTEM. 


27 


raG.  or  HOOT  opPneumog.^ 

T»  PETROSAL  e.  0, 

Glosso-p// 

fkOM  1^  CER  vicalN^ 
2*. 


iGAHOllON  or  niB£S 

\CAROriD  PLtiUS 

'  '"^NTf  0.      TO  5\''N. 

<l*  VIDIAN  roS-PQAN&uoii 


lARGCS.PerROSAL  TV 


CAKDIAC  BR.FR.  PNCUMOdASfRIC 
AMD  RB.C   LARYNGEAL   NERVES 


L.CQRONARY  PLEXUS 


G--  GANGLION 
P=  PLEXUS 
A--  ARTERY 
l,Z.3,^.  BRANCHES 
FROM  PNEUMQGA^TRIC 
NERVE    TO    THE 
CARDIAC  PLEXUS 


CYSTIC 

Gastro-ouodehal 


S  SUP.  HEM  OK  n  HOIOAt 
6  SPERMATIC  PLEXUS 


PBon  COCCY6OAL 


^^ffiV/^P.  OR  INF.HYPOGASTRIC 

^^^^upplies  all  thePelvic  viscera 
r=Sr^^:   and  the  Pents 


6ANSLION  IMPAR. 


FIG.  24. 
The  sympathetic  system  of  nerves. 


28  DISEASES   OF   THE   NERVOUS   SYSTEM. 

lying  upon  the  sides  of  the  vertebral  bodies,  there  are 
prevertebral  or  collateral  ganglia  placed  in  the  median 
line  of  the  ventral  spinal  surface,  such  as  the  semi-lunar, 
inferior  mesenteric,  etc.,  all  of  which  are  likewise  closely 
united  to  the  double  lateral  series. 

Fibres  from  both  the  anterior  and  posterior  roots  of 
the  spinal  nerves  pass  into  the  corresponding  ganglia, 
and,  in  the  cephalic  region,  there  is  a  free  exchange  of 
fibres  between  the  cranial  nerves  and  the  sympathetic. 
The  largest  gangliated  plexuses  are  found  in  the  thoracic 
and  abdominal  cavities. 

All  the  vaso-motor  nerves  originate  in  the  cerebro- 
spinal axis,  and  leaving  the  spinal  cord  by  the  anterior 
roots,  as  fine  medullated  fibres,  proceed  to  the  lateral 
series  of  sympathetic  ganglia,  where  they  lose  their 
myeline  sheaths  before  being  distributed  to  their  vascular 
areas.  The  vaso-motor  nerves  appear  chiefly  in  the  roots 
of  the  dorsal  spinal  nerves.  The  vaso-dilator  nerves, 
on  the  other  hand,  originate  more  particularly  from  the 
cranio-cervical  and  sacral  regions. 

The  viscero-motor  nerves  leave  the  cord  in  the  upper 
cervical  region  and  descend  with  the  visceral  branches 
of  the  accessory  and  vagus  nerves  to  the  ganglia  of  the 
vagus  trunk,  where  they  lose  their  myeline  sheaths  and 
are  distributed  to  the  alimentary  canal,  the  peristaltic 
action  of  which  they  govern. 

The  sympathetic  system  has  certain  independent  func- 
tions which  are  performed  even  when  all  communication 
with  the  central  nervous  organs  is  cut  off,  such  as  the 
automatic  movements  of  the  heart,  the  intestines,  ureters, 
blood-  and  lymph-vessels,  fallopian  tubes,  and  uterus; 
but  these  functions  are  more  or  less  influenced  in  the 
way  of  inhibition  and  stimulation  by  fibres  from  the 
cerebro-spinal  system.     There  are  other  functions,  such 


THE   NERVOUS   SYSTEM. 


29 


as  the  sensory  function  of  the 
splanchnic  nerve,  which  are  depend- 
ent upon  the  integrity  and  union 
of  the  two  systems. 

Besides  the  vaso-motor  and  vaso- 
dilator nerves  supplying  the  vessels 
of  the  various  tissues  (the  brain 
probably  has  no  vaso-constrictor 
nerves)  and  viscera  of  the  body, 
there  are  thought  to  be  secretory 
nerves  derived  from  the  sympathetic 
system,  governing  such  secretions 
as  the  tears,  saliva,  sweat,  mucus, 
digestive  juices,  urine,  etc.,  and 
there  is  in  a  measure  a  segmental 
representation  of  these  functions  in 
the  ganglionic  chain. 

One  of  the  sympathetic  functions 
which  is  of  practical  importance  for 
diagnostic  purposes  is  that  of  dilat- 
ing the  pupil.  The  cilio-spinal  cen- 
tre lies  in  the  cord  between  the 
fourth  cervical  and  second  dorsal 
segments,  and  the  pupil  -  dilating 
fibres  pass  thence  out  by  the  rami 
communicantes  into  the  cervical 
sympathetic,  which  conveys  them 
to  the  head.  Section  of  these  fibres 
causes  contraction  of  the  pupil,  and 
stimulation  dilatation. 

The  Motor  Tract. — We  may 
now  pass  to  the  consideration  of  the 
parts  of  the  nervous  system  that  are 
concerned  in  voluntary  motion. 


S'g 


<  -i ' 

/ 

^i 

£3 

h  < 

of  0 

\ 

V 

\ 

? 

<u  3 
|| 

— frt 

"  c 

a' 

=1 

Z 

lil 

0  iJ 

u. 

2 

•?« 

J 

0 

.2«-r 

4 

UJ 

(-<    r-    U5 

0 

10 

iut;  1-. 

*-■."    D 

2 
< 

LU 

ti 

a. 

i-(  -^  \^ 

> 

a 

0. 

0 

liJ 

a. 
0 
1- 

1 

.'2  0  2 

A 

s^ 

0 
)5 

0 

10          b   M-a 

1 

J?\  )7 

). 

—< 

z 

< 

2 

0 

r3  t^i  rt 

U3 

u  0  0 

bJ3^   " 
In  rt-O 

_    D    4) 
&>>« 

0  <j  5 

i;.-^ 

0  '-' 

or 

S  ="2 

QJ 

n  '3 

01 

(- 
■z 

«-c  0 

•£•3  ^ 

UJ 

UJ 

> 

0 

uJ 

(U    1)    > 

LU 

2 

•A 

»~^     t-t 

rj: 

Q: 

>^  0  en' 

0 

UJ 

c-c-p 

H 

5 

a. 

cj  i-n 

0 

0 

Ul 

1 

_) 

CD 

u> 

1  S  "" 

t<  s^  0 

m 

P 

ul 

— —1 

00 

^SH 

S°  : 

c  « 

30  DISEASES   OF  THE   NERVOUS   SYSTEM. 

Between  the  cortex  of  the  brain  of  one  side  and  the 
voluntary  muscles  of  the  opposite  side  of  the  body  lies  a 
system  of  fibres  which  we  call  the  motor-tract.  It  is  con- 
venient to  regard  this  tract  as  composed  of  two  neurons: 
one,  the  cerebro-spinal;  the  other,  the  spino-muscular. 

Each  cerebro-spinal  neuron  consists  of  a  cortical  por- 
tion, the  body  of  the  neuron,  and  a  spinal  portion,  its 
axis-cylinder  process,  which  terminates  by  communicat- 
ing with  the  spino-muscular  neuron  of  the  anterior  horn 
of  a  spinal  cord.  The  latter  terminates  by  means  of  its 
axis-cylinder  process  in  the  muscle-fibre  of  the  periphery. 

Let  us  study  the  topography  and  relations  of  these 
neuron  segments,  beginning  with  the  part  of  the  cortex 
especially  connected  with  voluntary  motion,  the  motor 
area.  This  area  comprises  the  ascending  frontal  and 
ascending  parietal  convolutions  bounding  the  Rolandic 
fissure  (sometimes  called  from  their  position  the  "cen- 
tral" convolutions),  the  superior  parietal  lobule,  the 
paracentral  lobule,  and  part  of  the  precuneus  {inde  Figs. 
7  and  8).  The  leg  muscles  are  mainly  represented  in 
the  upper  third  of  the  central  convolutions  and  in  the 
paracentral  lobule. 

The  arm  muscles  are  governed  from  the  middle  third 
of  these  central  convolutions  of  the  Rolandic  region. 
The  leg  and  arm  areas  probably  overlap  one  another. 

The  centre  for  the  movements  of  the  face  is  in  the 
lower  third  of  the  ascending  frontal  and  possibly  in  a 
portion  of  the  ascending  parietal  convolution. 

The  tongue  and  lips  are  represented  together  in  the 
lowest  part  of  the  ascending  frontal  convolution  and  in 
the  inferior  or  third  frontal  convolution,  and  it  is  not 
practicable  to  separate  their  regions,  because  of  the 
habitual  functional  association  of  the  orbicularis  oris  and 
transversus   linguae.     The  motor-area  for  speech  occu- 


THE   NERVOUS   SYSTEM.  3 1 

pies  about  the  same  position  as  the  centre  for  the  tongue 
and  lips;  that  is,  the  lower  or  third  frontal  convolution 
in  its  posterior  part.  These  areas  either  immediately 
adjoin  or  overlap  each  other,  but  the  motor-speech 
centre  is  usually  located  only   in  the  left  hemisphere. 

While  there  can  be  no  doubt  as  to  the  relation  existing 
between  the  parts  described  and  voluntary  motion,  it 
must  be  remembered  that  sensation,  also,  is  to  a  certain 
extent  localized  in  the  same  regions,  the  sensory  fibres 
from  the  periphery  terminating  by  communication  with 
special  neuron  types,  which  ultimately  carry  the  sensory 
impulse  over  to  the  motor  system  of  neurons.  The  sen- 
sory areas  and  tracts  will  be  discussed  in  a  subsequent 
paragraph.  ^ 

The  Rolandic  region  of  the  cortex  contains  the  largest 
neurons  in  the  central  nervous  system,  some  of  them 
being  as  much  as  65  //  in  diameter.  They  lie  in  what  is 
known  as  the  third  of  the  five  layers  of  the  cortex,  and 
their  bodies  have  a  pyramidal  shape,  with  their  apices 
toward  the  periphery  and  their  bases  directed  inward. 
From  the  bases  of  these  pyramids  spring  the  axis-cylinder 
process,  which  continues  uninterrupted  into  the  spinal 
cord,  w^here  it  communicates  with  the  spinal-neuron 
segment  of  the  anterior  horn.  The  motor  impulse  is 
thus  transmitted.  As  they  descend  toward  the  lower  part 
of  the  brain  these  fibres  converge  to  form  in  the  internal 
capsule  the  large  compact  bundle  of  the  motor  tract. 

The  internal  capsule  is  the  name  given  to  the  knee- 
shaped  mass  of  white  substance  seen  upon  making  a 
horizontal  section  of  the  brain  through  the  basal  ganglia. 
It  lies  between  the  nucleus  lenticularis  on  the  outside 
and  the  thalamus  and  nucleus  caudatus  on  the  inside. 
The  motor  tract  occupies  but  a  portion  of  the  internal 
capsule,  viz.,   the    anterior   two    thirds   of   the    portion 


32 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


behind  its  angle  or  knee  lying  between  the  optic  thalamus 
and  the  nucleus  lenticularis.  Before  reaching  the  internal 
capsule  the  fibres  for  the  leg,  arm,  and  face  hold  the 
same  relative  position   in   the  centrum  ovale  that  they 


FIG.  26. 

Horizontal  section  through  the  brain  showing  the  position  of  the  optic  thala- 
mus, the  corpora  striata  (caudate  and  lenticular  nuclei),  and  the  internal  capsule. 


have  upon  the  cortex — that  is,  from  the  median  line  out- 
wards, leg,  arm,  face — L  A  F.  As  the  bundles  enter 
the  internal  capsule  their  relative  positions  change  so 
that  L  A  F  is  the  formula  to  express  their  situation  from 


THE  NERVOUS   SYSTEM. 


33 


behind  forwards.  Their  positions  are  altered  again  as 
they  enter  the  crus  cerebri,  the  formula  L  A  F  showing 
their  relative  location  from  without  inwards,  for  the  leg 
bundle  is  outermost,  the  arm  bundle  next  in  order,  and 
the  face  bundle  nearest  the  median  line.  Thus  their 
situations  with  regard  to  the  median  line  are  completely 
reversed  in  their  progress 
from  the  cortex  to  the 
pons.  In  the  pons  the 
same  positions  are  main- 
tained until  the  facial 
bundle  crosses  to  its  nu- 
cleus on  the  opposite  side, 
and  a  little  lower  down  the 
tongue-fibres  cross  to  the 
hypoglossal  nucleus.  The 
leg  and  arm  bundles  con- 
tinue down  together  to 
form  the  remainder  of  the 
pyramidal  tract. 

The  motor  tracts  oc- 
cupy the  anterior  part  of 
the  pons  and  constitute  the 
anterior  pyramids  of  the 
medulla.  Just  as  they 
pass  from  the  medulla  to 
the  cord  most  of  the  fibres 
cross  to  the  opposite  side. 

The  number  of  fibres  which  decussate  to  enter  the  oppo- 
site lateral  column  of  the  spinal  cord  is  variously  esti- 
mated by  different  authors  at  from  seventy-five  to  ninety- 
seven  per  cent.  It  varies  considerably  in  different 
individuals.  The  remainder  of  the  fibres  of  the  motor 
tract  continue  down  into  the  anterior  column  of  the  same 


FIG.  27. 

Diagram  of  horizontal  section  through 
the  basal  ganglia  and  internal  capsule 
(left  side),  showing  the  position  of  the 
chief  tracts  in  the  internal  capsule. 
The  region  of  the  capsule  marked  by 
the  letters  L  A  F  is  occupied  by  motor 
fibres  :  L  corresponds  to  the  leg  fibres, 
A  to  the  arm  fibres,  F  to  the  face 
fibres  (including  fibres  to  face  muscles, 
and  tongue).  The  region  F-C  contains 
the  fronto-cerebellar  tract  (intellectual 
tract).  The  region  marked  S  contains 
the  general  sensory  tract  from  the 
opposite  side  and  the  fibres  from  the 
optic  and  olfactory  nerves  of  the  oppo- 
site side,  sometimes  called  the  "  sen- 
sory crossway." 


34 


DISEASES   OF  THE   NERVOUS   SYSTEM. 


INTERNAL     CftPiULE 
9 


side,  crossing  to  the  opposite  anterior  horns  at  various 
levels.     The  former  bundle   is   designated   the  crossed 
pyramidal  tract,  and  the  latter  the  direct  pyramidal  tract. 
There  is  good  reason  for  believing  that  the  crossed 
pyramidal  tract  is  destined  chiefly  for 
the  innervation  of  the  trunk  and  lower 
extremities,  and  the  direct  pyramidal 
tract  for  that  of  the  upper  extremi- 
ties; for  one  continues  to  the  lumbar 
enlargement,  and  the  other  generally 
disappears  in  the  mid-dorsal  region 
or  the  cervical  enlargement. 

We  have  now  traced  the  cerebro- 
spinal segment  of  the  motor  tract 
from  its  origin  in  the  cortex  to  its  ter- 
mination in  the  anterior  horns.  Its 
course  is  uninterrupted  throughout. 

Passing  to  the  consideration  of  the 
spino-muscular  portion  of  the  motor 
tract  we  have  to  examine  the  dis- 
position of  the  bodies  of  the  neurons 
in  the  anterior  horn.  These  are 
distributed  in  groups  or  clusters  in 
the  anterior  horns,  and  their  ar- 
rangement differs  in  the  various 
levels  of  the  spinal  cord.  We  dis- 
tinguish by  their  relative  position 
in  transverse  sections  at  certain 
levels  the  following  five  groups:  a 
median,  an  anterior,  an  antero-lat- 
eral,  a  postero-lateral,  and  a  central.     (Fig.  29). 

Often  the  second  and  third  of  these  are  not  distin- 
guishable from  one  another  by  any  well-marked  line  of 
separation. 


Diagram  showing  the 
position  of  the  pyramidal 
tract  of  the  right  side  at 
different  levels  of  the  brain 
and  in  the  spinal  cord. 
(After  Gowers.) 


THE   NERVOUS   SYSTEM. 


35 


The  occurrence  of  the  neurons  in  clusters  is  most 
marked  in  the  cervical  and  lumbar  enlargements.  In 
the  dorsal  region,  where  the  anterior  horns  are  small,  the 
distinction  of  isolated  groups  can  usually  be  made  out. 


Ul>per  Dorsal 


IGd-Lombar. 


FIG.   29. 


Diagrams  of  the  groups  of  nerve-cells  in  the  anterior  cornu.  Groups  :  I,  inner 
or  medial;  A,  anterior;  A.-L.,  antero-lateral ;  P.-L.,  postero-lateral  ;  I.  L.  P.,  inter- 
mediate lateral  process;  P.  V,  C,  posterior  vesicular  column  or  tract.  The  two 
mid-cervical  sections  are  only  a  few  millimetres  apart,  and  show  how  the  anterior 
group,  separate  in  the  one,  may  be  blended  with  the  antero-lateral  group  in  a 
neighboring  part  of  the  cord.     (Gowers.) 

A  knowledge  of  this  grouping  is  not  of  much  importance 
in  diagnosis,  for  we  have  not  yet  learned  of  the  exact  re- 
lationship existing  between  particular  neuron  aggrega- 
tions  and   the  muscles  which  they  govern.     We  know 


36 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


much  more   of  the  relations  of  the  masses  of  neurons 
taken   as   a   whole   in   the   anterior  horns   of  particular 


Columns  of  gray  matter  and  motor  nuclei  of  the  cervical  enlargement  (After 
F.  Sane).  Columna  medialis — i,  a,  short  rotators  of  head;  M.  subhyoid 
muscles;  i,  c,  d^  e^  f^  extensors  and  rotators  of  the  vertebral  column.  2, 
nucleus  diaphragmatis  (the  series  of  sympathetic  nuclei  composed  of  small  cells 
have  not  been  drawn  in),  they  are  situated  behind  the  column  medialis  near  the 
columna  canalis  centralis.  Columna  intermedio-lateralis — 8,  «,  accessorius  M. 
trapezius  and  M.  sterno-cleido  mastoideus;  b,  c,  plexus  cervicalis;  Mm.  trapezius 
sterno-cleido-mastoideus  ;  </,  ^,  middle  portion  of  M.  trapezius  ;  y,  inferior  part 
of  M.  trapezius  ;  <?,  beginning  of  the  nucleus  for  the  M.  latissimus  dorsi.  Columna 
extremitatis  superioris — 3,  Mm.  pectorales  ;  4,  b^  M.  levator  scapulae;  c,  M. 
serratus  major  ;  6,  muscles  of  the  shoulder ;  7,  t,  M.  biceps  ;  lower  down,  supina- 
tors and  extensors  of  the  fingers;  between  d  and  f,  flexors  and  pronators;  ^, 
thenar  and  hypothenar  muscles  ;  _/",  hypothenar  muscles  ;  5,  t/,  M.  triceps  bracnii; 
e^  M,  ancona:us.     (Barker.) 

segments  of  the  cord,  and  the  muscles  with  which  they 
are    connected.       There    are    probably,    also,    frequent 


THE  NERVOUS   SYSTEM. 


37 


FIG.  31, 


though  inconsiderable  variations  in  individuals,  as  re- 
gards the  extent  and  complexity  of  muscle  representation 
at  different  levels  of  the  cord.  It  should  be  noted  that 
muscle-groups  which  have  a  higher  position  in  the  body 
are  localized,  as  a  rule,  in 
higher  levels  of  the  cord. 
For  example,  the  shoulder 
muscles  have  their  spinal 
nuclei  in  the  upper  por- 
tion of  the  cervical  en- 
largement, while  the  hand 
muscles,  which  occupy  a 
lower  position  in  the 
body,  are  represented  in 

,        ,  •  r      1  Diagram  of  transverse  section  of  spinal 

the    lower    portion    01     the      cord,  showing  the  course  of  the  chief  sets 

of  fibres  in  the  nerve-roots.  (A.  anterior 
horn  ;  P.  posterior  horn.)  i  and  2.  Fibres 
which  enter  the  postero-external  column 
(Burdach)  and  take  an  ascending  or  de- 
scending course,  many  of  them  entering 
the  postero-median  column  (column  of 
Goll).  3.  Fibres  which  passto  the  cells 
of  the  column  of  Clarke,  which  in  turn 
send  fibres  to  the  direct  cerebellar  tract. 
4.  Fibres  passing  to  the  proper  sub- 
stance of  the  posterior  horn.  5.  Fibre 
coming  through  the  anterior  commissure 

lnrnli7Pitinn  plrpaHv  crivpn        ^""o™   ^^^   '^'^^^^^   pyramidal   tract   of   the 
lOCaJlZaUOnaireaay  given,      opposite   side.     6.    Fibre    coming  from  a 

4- Via  Ti^la-l-inn    r>f   fViA   rliffp'r        motor  ganglion-cell   of   the   opposite  an- 

tne  relation  ot  tne  amer-    ^^^^^^  g^^^     ^    ^.^^^  connected  with 

ent  muscles  to  the  various      motor  ganglion-cell  of  the  anterior  horn 

of  same  side.      1  his  gangliori-ceil  is  proba- 

SegmentS  of  the  cord  is  bly  connected  with  a  sensory  fibre  from 
°  the   opposite  posterior    horn.      8.    r  ibres 

Dresented.  from  motor  ganglion-cell  of  anterior  horn 

^  '  of  same  side.     Ihis  ganglion-cell  is  proba- 

The  neurons  of  the   an-     tly  connected  with   a  sensoryfibre  from 

the  posterior  horn  of  the  same  side.     9  and 

terior    horn     are     of     large     lo.    Fibres   from    the    crossed    pyramidal 

tract  of  the  same  side. 

Size,     the     axis  -  cylinder 

processes  of  which  collect  in  bundles  and  pass  through 
the  white  substance  to  emerge  as  the  anterior  roots  of 
spinal  nerves  from  the  cord.  When  joined  by  the  pos- 
terior or  sensory  root  at  the  intervertebral  foramen  it 
contributes  to  form  a  mixed  nerve — that  is,  one  having 


enlargement.  The  spinal 
representation  of  many 
of  the  larger  muscles  ex- 
tends through  several  seg- 
ments. 

In  the  table  of  spinal 


38 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


both  motor  and  sensory  fibres.  There  is  no  way  of  dis- 
tinguishing the  motor  from  the  sensory  fibres,  since  they 
have  no  characteristic  arrangement  in  the  spinal  nerves 
and  no  known  structural  differences. 

As  each  nerve  approaches  the  muscles  for  which  its 
motor  fibres  are  destined,  these  latter  leave  the  mixed 
nerve  in  bundles  to  enter  the  muscles  and  be  distributed 


FIG.   32, 
Motor  nerve-ending  of  intercostal  muscle-fibres  of  a  rabbit,     (Stohr.) 

to  their  fibrillae.      Each  nerve  fibril  terminates  in  a  mus- 
cular fibre  as  a  motorial  end-plate. 

The  Sensory  Tract. — We  know  far  less  of  the  ner- 
vous structures  that  subserve  ordinary  sensibility  than  of 
those  which  underlie  voluntary  motion,  and  the  difficul- 
ties of  tracing  the  sensory  paths  are  increased  by  the 
fact  that,  in  certain  parts  at  least,  different  forms  of 
sensation  are  conducted  by  different  structures.     The 


THE  NERVOUS   SYSTEM.  39 

skin  is  the  seat  of  a  variety  of  bodies  related  to  sensory 
perception.  Of  these  some,  like  corpuscles  of  Pacini 
and  Meissner,  and  the  end-bulbs  of  Krause,  are  differen- 
tiated tactile  organs  whose  office  it  is  to  modify  and 
possibly  to  multiply  the  effects  of  stimuli  upon  the  ter- 
minal nerve  filaments,  but  we  cannot  as  yet  ascribe 
specific  forms  of  sensory  function  to  these  different 
bodies. 

The  simpler  nervous  structures  in  the  skin  are  plexuses 
of  non-medullated  nerve-fibres  terminating  in  free  ex- 
tremities between  the  cells  of  the  mucosa,  and  are  more 
widely  distributed  than  the  end-organs  just  mentioned. 

There  is  some  reason  for  believing  that  these  various 
terminal  nerve-structures  respond  only  to  particular  kinds 
of  sensory  stimuli. 

Sensory  fibres  also  enter  the  muscles,  and  the  impres- 
sions conveyed  by  them  upon  contraction  of  the  muscle- 
fibres  have  much  to  do  with  the  sense  of  posture  and  the 
nice  control  and  proper  co-ordination  of  muscular  move- 
ments. 

There  are  good  reasons  for  believing  that  the  various 
sensations  of  touch,  pain,  temperature,  and  the  muscular 
sense,  have  special  terminal  filaments  for  their  appre- 
hension, and  possibly  for  their  conveyance  from  the 
periphery  to  the  central  nervous  system. 

In  the  intervertebral  foramen  all  of  the  sensory  fibres 
separate  from  the  motor  bundle  to  pass  into  the  spinal 
cord  as  the  posterior  root. 

The  fibres  composing  a  sensory  nerve  are  to  be  looked 
upon  as  the  dendrites  of  the  neuron,  the  body  of  which 
is  in  the  ganglion  of  the  sensory  root  with  its  axis- 
cylinder  process  in  the  spinal  cord.  The  first  neuron 
in  the  sensory  system  is,  therefore,  composed  of  a 
single  dendrite   which  extends  into   the  periphery   and 


40  DISEASES   OF  THE  NERVOUS   SYSTEM. 

appreciates  the  sensation,  a  body  which  is  located  in 
the  posterior-root  ganglion  and  an  axis-cylinder  process 
which  transmits  the  sensation  for  a  longer  or  shorter 
distance  in  the  spinal  cord.  This  anatomical  arrange- 
ment applies  to  all  sensory  nerves.  The  destination  of 
the  various  axis-cylinder  processes  entering  the  cord 
varies  considerably.  The  following  are  generally  distin- 
guished (see  Fig.  ^;^) :  A.  Fibres  ending  by  communication 
with  the  various  types  of  cells  found  in  the  posterior  horn. 
B.  Fibres  that  enter  the  posterior  columns  and  terminate 
by  communication  with  the  cells  of  the  nucleus  gracilis 
and  nucleus  cuneatus.  C.  Fibres  which  pass  to  the 
anterior-horn  cells  of  the  same  side  constituting  the 
direct  reflex  path  and  fibres  which  pass  to  the  opposite 
side  forming  a  bundle  which  transmits  the  sensations  of 
temperature  and  pain. 

Among  the  first  group  of  fibres  we  recognize,  besides 
those  terminating  in  the  cells  composing  the  gelatinous 
substance,  others  which  terminate  by  communication 
with  neurons  situated  at  the  base  of  the  posterior  horn. 
These  bodies  constitute  Clarke's  vesicular  column  and 
are  found  especially  well  marked  in  the  dorsal  and  upper 
lumbar  regions  of  the  spinal  cord.  They  exist  less 
pronounced  in  the  cervical  and  lower  lumbar  regions, 
where  they  are  known  as  Stilling's  column.  These  groups 
of  cells  are  of  great  importance  because  of  their  relation- 
ship to  the  direct  cerebellar  tract  which  lies  just  to  the 
outer  side  of  the  crossed  pyramidal  tract.  A  further 
tract  to  the  cerebellum  is  derived  from  neurons  lying  at 
the  base  and  at  the  junction  of  the  anterior  and  posterior 
horns  (Gowers'  bundle). 

The  second  (B)  group  of  fibres  mentioned  above  do 
not  terminate  till  they  reach  the  nucleus  gracilis  and 
nucleus  cuneatus  of  the  medulla. 


THE   NERVOUS   SYSTEM.  4I 

From  these  nuclei  the  sensory  system  is  continued  to 
the  brain  cortex,  on  the  one  hand,  by  the  formation  of 
the  lemniscus,  which  is  made  up  of  crossed  fibres  from 
these  nuclei,  and  to  the  cerebellum,  on  the  other,  by 
fibres  passing  by  way  of  the  restiform  body  to  the  cortex 
of  the  vermis.  Some  of  these  fibres  pass  direct,  without 
interruption  in  these  nuclei. 

Among  the  third  (C)  group  of  fibres  are  those  which 
pass  to  the  antero-lateral  cord  region  of  the  opposite  side 
and  which  transmit  pain  and  temperature  sensations. 
These  fibres  form  a  distinct  bundle  in  that  region  known 
as  the  fasciculus-spino-tectalis  et  thalamicum  (Horsley) 
fibres,  which  ultimately  find  their  way  into  the  lemniscus 
and  end  in  the  thalamus  opticus. 

We  see  that  the  path  and  distribution  of  a  sensory 
nerve  is  extremely  complex;  fibres  being  distributed  to 
and  ultimate  terminations  being  found  in  the  posterior 
horns  of  the  same  and  the  opposite  side  and  the  anterior 
horns  of  the  same  side  in  the  cord;  fibres  to  the  cerebel- 
lum which  are  interrupted  in  the  cord  (Clarke's  column) 
and  ftbres  to  the  cerebellum  which  are  interrupted  in 
the  medulla  (nuclei  gracilis  and  cuneatus),  fibres  which 
reach  the  basal  ganglia,  and  other  fibres  which  are  ulti- 
mately distributed  to  the  cerebral  cortex.  All  sensory 
nerves  are  thus  complex  and  in  addition  contain  also 
elements  belonging  to  the  so-called  sympathetic  system. 
Like  the  motor  tract  the  decussation  of  the  sensory  tract 
is  an  incomplete  one.  Much  of  this  decussation  takes 
place  in  the  spinal  cord,  but  rather  more  occurs  in  the 
medulla. 

As  regards  the  position  of  the  sensory  tract  in  the 
medulla,  pons,  and  brain  only  general  statements  can 
be  made. 

In  the  upper  portion   of  the  medulla  the  cerebellar 


42 


DISEASES   OF  THE   NERVOUS   SYSTEM. 


FIG.  33. 

Schematic  diagram  of  the  more  important  tracts  of  the  posterior  columns  of  the 
cord.  Gsp,  spinal  ganglion  (1,  lumbar,  d,  dorsal,  c,  cervical) ;  CCl,  Clarke's  col- 
umn ;  Ks,  cerebellar  tract  ;  G,  Coil's  column  ;  B,  Burdach's  column  ;  Ng,  nucleus 
gracilis;  Nc,  nucleus  cuneatus  ;  DLm,  decussation  of  the  lemniscus;  Crst,  resti- 
torni  body  ;  Narc,  nucleus  arcuatus  ;  Oi,  inferior  olive  ;  Os,  superior  olive  ;  Lnim, 
medial  lemniscus  ;  Lml,  lateral  lemniscus  ;  Nil,  nucleus  of  the  lateral  lemniscus  ; 
Qp,  Qa,  anterior  and  posterior  corpora  quadrigemina  ;  Tho,  optic  thalamus  ;  Cc, 
ci  rebral  cortex.      (Obersteiner.) 


THE   NERVOUS   SYSTEM.  43 

fibres  have  already  passed  to  their  destination,  and 
the  crossed  sensory  fibres  which  here  constitute  the 
lemniscus  or  fillet  are  only  to  be  considered.  They 
end  in  nuclei  belonging  to  the  optic  thalamus  and 
ultimately  reach  the  cortex  in  all  probability  through 
various  groups  of  fibres  known  as  the  inferior,  an- 
terior, posterior,  and  external  radiators  of  the  thala- 
mus. Another  group  of  sensory  fibres  occupies  the 
posterior  third  of  the  posterior  limb  of  the  internal  cap- 
sule, a  position  immediately  behind  and  contiguous  to 
the  motor  tract.  The  cortical  termination  is  probably 
in  the  ascending  frontal  and  ascending  parietal  convolu- 
tions and  contiguous  areas  of  the  parietal  lobe. 

From  what  has  gone  before  it  will  be  seen  that  certain 
of  the  sensory  fibres  cross  to  the  opposite  side  in  the 
cord  (temperature  and  pain),  while  certain  others  (tactile 
and  muscle  sense)  remain  uncrossed  till  they  reach  the 
medulla.  From  this  circumstance  is  made  possible  the 
symptom-complex  of  Brown-Sequard's  paralysis. 

It  is  probable  that  the  fibres  making  up  the  posterior 
columns  transmit  certain  muscular  impulses,  as  well  as 
tactile  sense  and  muscle  pain  sense. 

Reflex  Paths. — A  reflex  movement  of  the  simplest 
kind  may  be  imperfectly  defined  as  one  that  results  from 
the  conversion  or  "  reflexion  "  of  a  sensory  stimulus  into 
a  motor  excitation.  A  sensory  or  afferent  impulse  is 
conveyed  centrally  by  a  sensory  neuron  to  a  motor 
neuron,  whence  it  is  reflected  outward  along  a  motor 
nerve  to  a  muscle  or  group  of  muscles. 

Thus  the  integrity  of  two  neurons  is  necessary  in 
order  to  make  possible  reflex  action,  a  sensory  neuron  on 
the  one  hand  and  a  motor  neuron  on  the  other,  and  such 
a  combination  constitutes  a  "reflex  arc."  The  motor 
element  in  this"  arc"  is  known  as  the  "reflex  centre," 
and  these  are  the  same  neurons  as  those  constituting  the 


44  DISEASES   OF   THE   NERVOUS   SYSTEM. 

final  link  in  the  cerebro-spinal  motor  system,  under 
which  circumstances  they  act  as  transmitters  of  voluntary 
motor  impulses  descending  from  the  cortex. 

The  upper  neuron  elements  in  the  motor  system  do 
more  than  conduct  voluntary  impulses  from  the  brain 
to  the  lower  neuron  group,  in  that  they  exercise  a  re- 
straining or  inhibitory  influence  upon  the  elements  of 
the  reflex  arc,  more  particularly  its  motor  element.  If, 
therefore,  the  upper  neuron  is  injured  or  destroyed,  as 
occurs,  for  example,  in  lesions  of  the  internal  capsule  or 
disease  of  the  motor  cortex  or  the  crossed  pyramidal 
tracts,  this  inhibitory  influence  is  removed,  the  activity 
of  the  reflex  centre  is  uncontrolled,  and  the  motor 
phenomenon  becomes  exaggerated.  This  applies  par- 
ticularly to  the  deep  tendon  reflexes. 

The  gray  substance  of  the  spinal  cord  contains  a  series 
of  reflex  centres,  cutaneous,  muscular,  and  visceral. 
Some  are  complex  and  of  considerable  vertical  extent. 
The  relations  of  the  more  important  reflexes  to  particu- 
lar segments  are  given  in  the  table  of  localization  of  the 
functions  of  the  spinal  cord.  The  technique  of  their 
examination  will  be  dwelt  upon  in  another  chapter. 

The  Spinal  Nerves. — There  are  thirty-two  pairs  of 
spinal  nerves.  They  arise  at  nearly  equal  intervals  be- 
tween the  conus  medullaris  and  the  medulla.  Each 
nerve  is  formed  by  the  junction  of  an  anterior  (motor) 
and  a  posterior  (sensory)  root,  and,  leaving  the  spinal 
canal  through  the  intervertebral  foramen  as  a  mixed 
nerve,  soon  divides  into  two  branches,  an  anterior  and 
a  posterior.  These  branches  either  join  with  others  in 
the  formation  of  plexuses  from  which  arise  new  nerve- 
trunks,  or  pass  directly  to  their  cutaneous,  muscular,  or 
visceral  distribution.  The  nerve-roots  differ  in  size  at 
various  levels  of  the  cord,  those  of  the  dorsal  region, 
for  instance,  being  smaller  than  those  of  the  lower  cervi- 


THE   NERVOUS    SYSTEM. 


45 


FIG.  34- 


46 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


til 


snx3id  iJVQi^ni 


snx3id  ivyovs 


FIG.  35. 


THE  NERVOUS   SYSTEM.  47 

cal  and  lumbar  regions,  and  this  leads  to  inequalities  of 
size  in  the  nerve-trunks  formed  by  them. 

The  spinal  nerves  give  rise  to  three  plexuses  of  cardinal 
importance,  known  as  the  brachial,  lumbar,  and  sacral. 

The  brachial  plexus  is  formed  by  the  interlacing  of  the 
anterior  branches  of  the  spinal  nerves  arising  from  the 
four  lower  cervical  and  first  dorsal  segments  of  the  cord. 
There  is  also  a  small  communicating  branch  from  the 
fourth  cervical  nerve.  The  manner  of  their  union  to 
form  the  outer,  posterior,  and  inner  cords  of  the  plexus, 
and  the  subsequent  division  of  these  trunks  into  the  great 
peripheral  nerves  of  the  upper  extremity,  are  best  seen 
in  the  accompanying  illustration  (Fig.  34).  In  the  table. 
of  localization  of  the  functions  of  the  spinal  cord  an 
attempt  has  been  made  to  show  the  relations  of  the  more 
important  peripheral  nerves  to  their  segments. 

The  lumbar  plexus  is  derived  from  the  anterior  branches 
of  the  last  dorsal  and  first  four  lumbar  nerves,  and  the 
manner  of  their  union  and  the  chief  nerve-trunks  which 
arise  from  it  are  shown  in  the  accompanying  diagram 

(Fig.  35). 

The  sacral  plexus^  formed,  as  shown  in  the  diagram 

(Fig.  35),  from  the  last  lumbar  and  four  sacral  nerves, 
gives  rise  to  the  great  trunk  of  the  sciatic. 

The  Cranial  Nerves. — There  are  twelve  pairs  of 
cranial  nerves  which  leave  the  base  of  the  brain  at  un- 
equal intervals,  thus  contrasting  with  the  regularity  of 
arrangement  ot  the  spinal  nerves.  Like  the  spinal 
nerves,  which  arise  from  the  gray  matter  around  the 
central  canal  of  the  cord,  the  cranial  nerves  take  their 
origin  from  clusters  of  ganglion-cells  which  occur  in  the 
gray  matter  irregularly  disposed  about  the  cavities  in 
the  medulla,  pons,  and  crus,  these  cavities  (the  fourth 
ventricle  and  the  aqueduct  of  Sylvius)  being  merely 
continuations  upward  of  the  central  canal  of  the  cord. 


48  DISEASES   OF   THE   NERVOUS   SYSTEM. 

Leaving  their  nuclei  of  origin,  the  fibres  constituting 
the  various  cranial  nerves  pass,  by  more  or  less  direct 
paths,  to  the  base  of  the  brain,  to  emerge  at  points 
known  as  their  superficial  origins.  From  here  to  their 
foramina  of  exit  the  nerve-trunks  are  of  different  lengths 
and  their  relative  disposition  is  such  that  pathological 
processes  at  the  base  of  the  brain  produce  very  different 
and  valuable  localizing  symptoms.  Indeed,  a  clear 
picture  of  the  position  of  the  nuclei  and  of  the  arrange- 
ment of  the  intracranial  courses  of  these  nerves  is  of  the 
greatest  importance  for  diagnosis.  For  instance,  in  the 
diagram  of  the  origins  of  the  cranial  nerves  (Fig.  17)  it 
will  be  seen  that  a  lesion  at  the  side  and  upper  part  of 
the  medulla  might  involve  six  of  the  most  important 
trunks;  that  the  long  course  of  the  sixth  pair  over  the 
pons  renders  them  very  susceptible  to  injury;  and,  again, 
that  some  pairs,  like  the  optic  nerves  at  the  chiasm,  the 
third  nerves,  and  the  sixth  pair,  may  be  very  readily 
affected  together  because  of  their  nearness,  or,  on  the 
other  hand,  that  others  may  be  seldom  affected  because 
of  their  wide  separation  at  their  superficial  origin,  as  in 
the  case  both  of  the  fourth  and  fifth  pairs. 

We  now  pass  to  the  discussion  of  the  entire  course  of 
each  of  these  nerves. 

The  First  or  Olfactory  Nerve. — Our  knowledge  of  this 
nerve  and  its  central  connections  is  meagre.  The  per- 
ipheral filaments  from  the  Schneiderian  membrane  pass 
through  the  numerous  foramina  of  the  ethmoid  bone  into 
the  olfactory  bulb  lying  along  the  under  surface  of  the 
frontal  bone.  From  this  bulb  the  olfactory  nerve  passes 
backward,  dividing  into  three  roots.  The  fibres  of  the 
external  root  pass  into  the  temporo-sphenoidal  lobe  of 
the  same  side  and  disappear  in  the  anterior  part  of  the 
uncinate  gyrus,  which  is  probably  the  cortical  area  for 
the  sense  of  smell.     The  fibres  of  the  middle  root  dis- 


THE   NERVOUS   SYSTEM. 


49 


appear  in  the  anterior  perforated  space,  while  those  of 
the  inner  root  pass  to  the  anterior  cerebral  commissure. 
There  is  good  reason  for  believing  that  each  olfactory 
nerve  is  connected  with  the  cortical  areas  for  smell  of 


FIG.   36. 

The  olfactory  bulb  and  tract.  A,  Schneiderian  membrane  in  nose  in  which  lies 
peripheral  olfactory  neuron  ;  B,  glomerulus  of  olfactory  bulb  ;  C,  mitral  cells 
with  dendrites  in  B,  and  axones  in  D,  olfactory  lobe ;  E,  granule  cells  ;  F,  cells  in 
olfactory  lobe;  H,  G,  fibres  of  olfactory  tract.     (Ramon  y  Cajal.) 


both  hemispheres,  but  the  exact  paths  of  these  connect- 
ing fibres  are  not  yet  known. 

The  Second  or  Optic  Nerve. — The  nerve  of  sight  is  far 
more  important  in  its  diagnostic  relations.  Passing  back- 
ward from  the  retina,  the  optic  nerve  undergoes  partial 
decussation,  the  fibres  from  the  nasal  half  of  the  fundus 
crossing  to  the  opposite  side.  The  nasal  half  of  the 
retina  corresponds  to  the  temporal  half  of  the  field  of 
vision,  and  as  it  is  larger  than  the  temporal  half  of  the 
retina,  owing  to  the  limitation  of  the  nasaL visual  field  by 
the  projecting  nose,  a  greater  number  of  fibres  decussate 
than  follow  the  direct  path. 

The  amount  of  decussation  varies  somewhat  in  differ- 
ent animals  and  in  individuals.  In  the  chiasm  we  recog- 
nize three  groups  of  fibres  :  (i)  The  decussating  fibres 


50  DISEASES   OF  THE   NERVOUS   SYSTEM. 

mentioned  above  (from  the  nasal  side  of  the  retina);  (2) 
non-decussating  fibres  from  the  temporal  side  of  the  ret- 
ina ;  (3)  fibres  passing  between  the  two  optic  tracts  and 
which  have  no  connection  with  the  retina.   (See  Fig.  37  ) 

After  leaving  the  chiasm  these  varied  fibres  form  what 
is  known  as  the  optic  tract.  The  crossed  fibres  occupy 
the  lower  portion  of  the  tract,  the  non-decussating  fibres 
the  upper  portion,  while  the  intertractal  fibres  lie  pos- 
teriorly. 

Near  the  posterior  part  of  the  thalamus  the  tract 
divides  into  two  unequal  parts,  the  outer  being  the  larger 
and  being  distributed  chiefly  to  the  external  geniculate 
body  and  the  pulvinar  of  the  thalamus.  About  seventy 
per  cent,  of  the  tract  fibres  end  thus.  The  fibres  of  the 
inner  division  end  in  the  anterior  corpora  quadrigemina 
and  constitute  about  twenty  to  thirty  per  cent,  of  the 
tract  fibres.  These  endings  are  to  be  looked  upon  as 
the  points  of  termiijation  of  the  second  neuron  in  this 
particular  sensory  system.  The  first  neuron  lies  entirely 
within  the  retina. 

From  these  various  points  the  second  neuron  completes 
the  system  to  the  cortex,  the  fibres  being  gathered  into 
a  considerable  bundle,  the  anterior  arm  of  the  corpora 
quadrigemina.  These  fibres  pass  to  the  most  posterior 
portion  of  the  internal  capsule  and  finally  reach  the  cor- 
tex through  the  optic  radiation. 

A  few  fibres  probably  reach  the  cortex  without  inter- 
ruption in  the  basal  ganglia. 

The  cortical  areas  in  which  the  optic  radiation  termi- 
nates are  certain  portions  of  the  occipital  lobe,  outer 
aspect,  the  cuneus,  and  certain  areas  about  the  calcarine 
fissure. 

If  it  is  the  right  optic  path  that  is  affected,  the  right 
retinal    halves   become   blind.     Hemianopsia  has   been 


THE  NERVOUS   SYSTEM. 


51 


caused  by  diseases  of  the  apex,   external  surface,   and 
internal  surface  of  the  occipital  lobe,  but  is  most  com- 


Schematic  diagram  of  the  central  origin  of  the  optic  nerve.  R,  retina— dark 
portion  derives  its  nerve  supply  from  the  left,  while  the  light  portion  is  supplied 
from  the  right  hemisphere;  No,  optic  nerve;  Tro,  optic  tract  ;  CM,  Meynent  s 
commissure  :  Cg,  Gudden's  commissure  ;  1,  lateral  root  tract ;  m,  medial  root  tract; 
Tho,  optic  thalamus  ;  Cgl,  lateral  geniculate  body  ;  Qa,  anterior  corpora  quad- 
rigemina;  Rd,  direct  root  tract  to  the  cortex ;  Sm,  optic  radiation  to  the  occipital 
lobes  ;  Co,  posterior  occipital  cortex.     (Obersteiner.) 

mon  when  the  cuneus  is  involved  ;  and  it  may  be,  when 
other  occipital  areas  than  the  cuneus  are  invaded  with 


52  DISEASES   OF  THE   NERVOUS   SYSTEM. 

resulting  hemianopsia,  that  the  underlying  fibres  of  the 
optic  radiations  are  included  in  the  lesion. 

The  Third^  Fourth^  and  Sixth  Nerves. — These  nerves 
are  all  closely  associated  in  the  innervation  of  the 
muscles  which  move  the  eyeball,  and  the  third  (or  oculo- 
motorius)  supplies  also  the  internal  muscles  of  the  eye, 
namely,  the  sphincter  iridis  and  ciliarius.  The  muscles 
controlled  by  the  third  nerve  are  the  sphincter  iridis, 
superior  rectus,  inferior  rectus,  internal  rectus,  levator 
palpebrae,  and  inferior  oblique. 

The  individual  nerve-fibres  from  these  muscles,  after 
passing  through  the  optic  foramen  and  along  the  cavern- 
ous sinus,  unite  into  a  trunk  of  considerable  size,  which 
winds  over  the  crus  cerebri  to  disappear  between  the  two 
crura,  very  close  to  its  mate  of  the  opposite  side.  The 
liability  of  the  third  pair  to  suffer  together  because  of 
this  nearness  of  their  superficial  origins  has  already  been 
mentioned.  Entering  the  tegmentum  just  internal  to  the 
crus,  the  fibres  of  the  oculo-motorius  pass  through,  and 
by  the  cluster-of  cells  known  as  the  red  nucleus  (nucleus 
ruber),  to  some  nests  of  ganglion-cells  lying  in  the  in- 
terior of  the  gray  matter  below  the  aqueduct  of  Sylvius, 
at  a  point  just  under  the  region  of  the  anterior  corpora 
quadrigemina.  The  general  nucleus  of  the  oculo- 
motorius  is  known  to  consist  of  a  series  of  nuclei  each 
of  which  represents  some  one  of  the  muscles  innervated 
by  the  nerve,  and  their  relative  arrangement  from  before 
backward  is  probably  very  nearly  as  follows:  Rectus  in- 
ferior, obliqus  inferior,  rectus  internus,  rectus  superior, 
levator  palpebrae.  (See  Fig.  38.)  The  cell  group  bear- 
ing relationship  to  the  ciliary  muscles  of  the  iris  is  prob- 
ably separate  from  the  others  and  is  constituted  in  a 
group  known  as  the  Edinger-Westphal  nucleus,  the  two 
halves  of  which  are  situated  near  the  median  line. 


THE   NERVOUS    SYSTEM. 


53 


The  arrangement  of  the  muscle  representation  in  the 
nucleus  from  without  inward  is  also  shown  in  the  dia- 
gram of  the  accompanying  sagittal  projection. 

The  Fourth  Nerve  or  Patheticus. — The  fourth  nerve, 
controlling  the  action  of  the  superior  oblique  muscle, 
lies  upon  the  outer  side  of  the  cavernous  sinus  in  com- 
pany with  the  branches  of  the  third  nerve,  and  is  hence 
apt  to  suffer  with  it  in  lesions  affecting  this  region.     The 


FIG.  38. 


Scheme  of  the  oculo-motor  nucleus  (modified  after  Bemheimer"),  sagittal  projec- 
tion.    M,  median  nucleus  ;  EW,  Edinger-Westphal's  nucleus.    (Obersteiner.) 

superficial  origin  of  this  nerve  is  in  the  valve  of  Vieus- 
sens,  in  the  roof  of  the  fourth  ventricle,  the  nerve  ap- 
pearing on  the  surface  just  external  to  the  crus  cerebri, 
and  on  a  level  with  the  upper  border  of  the  pons. 

Within  the  substance  of  the  valve  there  is  a  decussa- 
tion of  the  fourth  pair  of  nerves.  It  is  probable  that  all 
of  the  fibres  take  part  in  this  decussation.  Then  the 
fibre-bundles  pass  downwards  and  forwards  around  the 


54 


DISEASES   OF  THE   NERVOUS   SYSTEM. 


Sylvian   aqueduct   to  the  gray  matter  in  its  floor,  just 
posterior  to  the  nuclei  of  the  third  nerve. 

The  Sixth  Nerve  or  Abducens. — This  nerve  supplies 
the  external  rectus  and  probably  gives  some  fibres  also 
to  the  internal  rectus.  In  the  cavernous  sinus  it  lies 
beside  the  fibre-bundles  of  the  third  and  fourth  nerves. 


FIG.  39. 

Scheme  of  the  oculomotor  nucleus  (modified  after  Bernheimer"),  basal  projec- 
tion.    M,  median  nucleus  ;  EW,  Edinger-Westphal's  nucleus.     (Obersteiner.) 

From  here  it  takes  a  long  course  over  the  prominent 
convex  surface  of  the  pons  (thus  rendering  it  very  liable 
to  suffer  compression,  especially  from  sub-tentorial 
growths)  to  its  superficial  origin  between  the  lower  pon- 
tine border  and  the  pyramid  of  the  medulla,  not  far 
from  the  median  line.     Both  nerves  often  suffer  together 


THE   NERVOUS   SYSTEM. 


55 


because  of  their  nearness  to  each  other  in  their  origin 
and  course,  and  lesions  at  the  base  of  the  brain  some- 
times involve  one  of  the  sixth  nerves  together  with  the 
fifth,  for  the  abducens  passes  very  close  to  the  superficial 
origin  of  the  latter  in  its  course  over  the  pons. 


RetT.  eoPY 


FIG.  40. 

Diagram  of  section  through  lower  part  of  pons.  This  diagram  is  not  quite 
accurate,  as  it  represents,  for  convenience,  certain  structures  which  are  not  actually 
observed  at  exactly  the  same  level.  (Thus  it  shows  the  origin,  course,  and  exit  of 
the  7th  nerve.)  VI,  abducens  nerve  and  nucleus  ;  N  VII,  nucleus  of  facial  nerve ; 
VII,  facial  nerve;  VIII  ant.  and  VIII  post.,  anterior  and  posterior  or  deep  and 
superficial  roots  of  the  auditory  nerve ;  Corp.  Rest.,  restiform  body  :  Knee,  knee 
of  the  facial  nerve  ;  O.  S.,  superior  olive  ;  P.L.B.,  posterior  longitudinal  bundle  ; 
S.T.F,,  superficial  transverse  fibres  of  the  pons  ;  D.T.F.,  deep  transverse  fibres  of 
pons ;  V.  Asc,  ascending  root  of  trigeminus  ;  Sub.  Gel.,  substantia  gelatinosa. 
The  internal  or  "  chief  "  auditory  nucleus  lies  just  internal  to  the  nucleus  of 
Deiter's. 

The  central  origin  of  the  si'xth  nerve  is  from  a  small 
nucleus  immediately  below  the  floor  of  the  fourth  ven- 
tricle, beneath  the  eminentia  teres  and  in  front  of  the 
striae  acusticae.  A  transverse  section  of  the  pons  at 
this  level  shows  the  seventh  nerve  curving  about   this 


56 


DISEASES   OF  THE   NERVOUS   SYSTEM. 


nucleus  of  the  sixth  nerve,  and  these  two  nerves  are 
sometimes  affected  together  by  a  lesion.  When  they 
are  thus  involved,  and  without  including  the  eighth 
nerve,  disease  of  the  pons  is  indicated.  There  is  no 
direct  anatomical  connection  between  the  nuclei  of  the 
sixth  and  seventh  nerve  as  formerly  supposed. 

The  three  ocular  nerves,  the  third,  fourth,  and  sixth, 
have  so  close  a  physiological  association  that  it  would  be 
natural  to  expect  considerable  proximity  of  their  nuclei. 

But  the  whole  length  of  the  pons  lies 
between  the  cell-nests  of  the  third 
and  fourth  nerves  and  the  nucleus 
of  the  sixth.  These  various  nuclei 
are,  however,  associated  together 
by  means  of  association-fibres  lying 
in  the  tract  known  as  the  posterior 
longitudinal  bundle  which  runs  near 
the  posterior  surface  of  the  pons 
adjacent  to  the  median  line  upward 
from  the  medulla  to  the  gray  matter 
of  the  third  ventricle.  These  fibres 
Pj^  subserve  the  conjugate  movement 

Diagram  of  the  mechanism     of  the  CyCS  from  side  tO  side,   for  in 

for  the  associated   lateral   guch  movemcuts  the  external  rectus 

movement  of  the  eye.  (Gow- 

^"■^•^  of  one  eye  (supplied  by  the  sixth 

nerve)  and  the  internal  rectus  of  the  other  eye  (supplied 
by  the  third  nerve)  must  act  simultaneously,  as  shown  in 

Fig.  43- 

It  is  highly  probable  that  these  muscle  groups  have  a 
bilateral  cortical  representation.  That  is,  each  muscle 
is  represented  on  both  sides  in  the  cerebral  cortex.  This 
is  true  of  some  other  muscle  groups  as  well,  such  as  the 
upper  facial  and  the  back  muscles.  In  fact,  the  law  of 
bilateral  representation  seems  to  apply  to  certain  muscle 


THE   NERVOUS    SYSTEM.  57 

groups  capable  of  being  used  voluntarily,  but  under  con- 
stant usage  having  passed  from  under  the  immediate 
control  of  the  will.  We  are  thus  enabled  to  understand 
why  complete  paralysis  of  these  muscles  of  cortical  origin 
is  never  seen. 

No  definite  cortical  area  for  this  group  of  muscles  is 
positively  known.  Paresis  of  the  levator  palpebrae  fol- 
lowing lesions  of  the  angular  gyrus  of  the  opposite  side 
has  led  to  the  association  of  this  area  with  this  muscle. 

The  Fifth  Nerve  or  Trigeminus. — This  nerve  is  both 
motor  and  sensory  in  function.  Its  motor  fibres  inner- 
vate the  muscles  which  move  the  jaw.  It  gives  sensory 
fibres  to  all  parts  of  the  face,  conjunctiva,  nasal,  oral, 
pharyngeal,  and  buccal  cavities,  to  the  tongue,  and  to 
the  dura  mater.  In  fact,  it  is  the  sensory  nerve  for  all 
of  those  parts  whose  movements  are  governed  by  the 
several  motor-cranial  nerves  from  the  hypoglossal  to  the 
oculo-motorius.  Moreover,  it  contains  fibres  which  sub- 
serve the  sense  of  taste. 

The  three  branches  which  have  given  it  the  name  of 
trigeminus,  viz.,  the  ophthalmic  and  superior  and  in- 
ferior maxillary  nerves,  unite  into  one  great  trunk,  about 
an  inch  from  the  superficial  origin  of  the  nerve,  upon 
meeting  in  the  Gasserian  ganglion.  The  inferior  maxil- 
lary branch  contains  all  the  motor  fibres  (see  Fig.  44). 
The  sensory  root  enters  the  pons  in  close  company  with 
the  motor  root  about  the  middle  of  the  pons,  but  at  some 
distance  from  the  median  line.  The  origins  of  this  pair  of 
nerves  are  the  most  widely  separated  of  any  of  the  cranial 
nerves,  and  to  this  is  due  the  rarity  of  their  involvement 
together  in  any  one  lesion.  They  are  also  quite  remote 
from  the  roots  of  other  nerves,  the  nearest  being  those  of 
the  fourth  and  sixth. 

The   nuclear   origin  of  the  fifth  nerve  is   very  com- 


58 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


plex  as  shown  in  Fig.  43,  particularly  in  its  sensory 
portion.  The  sensory  root  passes  backward  and  in- 
ward through  the  outer  part  of  the  pons  to  some  small 
groups  of  cells   lying  beneath  the  floor  of  the   fourth 


FIG.  42, 

Fifth  nerve  or  trigeminus. 


ventricle  known  as  the  middle  nucleus.  The  majority 
of  the  fibres,  however,  turn  downwards  through  the 
pons  and  medulla  under  the  name  of  the  descending 
root.  This  root  lies  just  internally  to  the  restiform 
body,  and,  growing  smaller  as  it  passes  downwards,  term- 


THE   NERVOUS   SYSTEM. 


59 


mates  in  the  upper  part  of  the  spinal  cord  in  close  con- 
nection   with    the    upper    expansion    of    the    gelatinous 


FIG.  43- 

Scheme  of  the  central  course  of  the  trigeminal  nerve.  Rs,  sensory  root ;  Rm, 
motor  root ;  Rsp,  spinal  root  ;  Re,  cerebral  root  ;  Ns,  sensory  nucleus  ;  Sg,  sub- 
stantia gelatinosa ;  Nm,  motor  nucleus ;  Sf ,  substantia  ferruginea  ;  Ra,  raphe. 
(Obersteiner.) 

substance  of  the  posterior  horn  (the  gray  tubercle  of 
Rolando). 


6o  DISEASES   OF   THE   NERVOUS   SYSTEM. 

The  descending  root  consists  of  several  small  bundles 
which  may  be  traced  from  the  level  of  the  middle  nucleus 
in  an  upward  direction  as  high  as  the  upper  part  of  the 
corpora  quadrigemina,  where  they  arise  from  large  round 
nerve-cells.  These  lie  external  to  the  aqueduct  of 
Sylvius  and  are  arranged  in  the  form  of  a  crescent. 


FIG.  44. 

Diagram  of  section  through  middle  of  pons,  showing  origin  of  the  trigeminus. 
V  Sens.,  sensory  nucleus  of  the  fifth  ;  V  M,  motor  nucleus  of  fifth  ;  M  Root, 
motor  root  of  fifth;  V,  fifth  nerve  ;  P.L.B.,  posterior  longitudinal  bundle. 

V  D,  Descending  root  of  fifth  nerve  ("  trophic  "  root). 


The  majority  of  the  fibres  of  the  motor  root  arise  from 
a  collection  of  large  ganglion-cells  of  limited  vertical  ex- 
tent which  lies  just  internal  to  the  sensory  root  of  the 
fifth  nerve  in  the  lateral  part  of  the  tegmentum  of  the  pons. 

There  are  many  intricate  arrangements  of  the  sensory 
portion    of   this    nerve.     Its   so-called   descending  root 


THE   NERVOUS   SYSTEM. 


6l 


corresponds  to  the  Rolandic  substance  of  the  posterior 
horns  of  the  spinal  cord  and  really  consists  of  small  cells 
from  which  the  sensory  fibres  destined  ultimately  to  join 
the  great  sensory  tract,  the  lemniscus,  take  their  origin. 


G.S.P. 


lC-\  ~^s!s^ 


€^ 


Aud, 


Post  A  u. 


FIG.   45. 

Diagram  of  facial  nerve  and  its  connections  (modified  from  Leube),  showing 
course  of  taste  fibres.  V,  trigeminal  nerve;  i,  2,  3,  first,  second,  and  third 
divisions  of  trigeminus;  F,  facial  nerve  ;  Aud,  auditory  nerve;  G.  S.  P.,  great 
superficial  petrosal;  S.  S.  P.,  small  superficial  petrosal;  Gen,  geniculate  ganglion; 
Ot,  otic  ganglion;  M,  Meckel's  ganglion  ;  Uv,  uvula;  L,  lingual  nerve;  C.  T., 
chorda  tympani ;  Stap,  nerve  to  stapedius;  St.  M.,  stylo-mastoid  foramen  ;  Post. 
A.U.,  posterior  auricular  nerve;  G.  P.,  glosso-pharyngeal  nerve;  P_,  petrous 
ganglion  of  glosso-pharyngeal;  Jac,  Jacobson's  nerve;  Car,  tympanic  plexus 
near  carotid  artery.  , 

N.  B.— Dotted  line  =  taste  fibres  from  anterior  two  thirds  of  tongue  ;  dash  line 
=  taste  fibres  from  posterior  third  of  tongue.     (AUchin.) 

The  distribution  of  the  sensory  fibres  so  originating  forms 
no  exception  to  the  disposition  of  the  sensory  system 
generally,  as  already  described.     There  is  a  partial  de- 


62  DISEASES   OF   THE   NERVOUS   SYSTEM. 

cussation  of  the  tract  so  formed,  a  considerable  portion 
passing  to  the  opposite  side,  the  fibres  ultimately  joining 
the  lemniscus  in  the  region  of  the  red  nucleus.  Fibres 
from  the  same  side  also  pass  to  the  cerebellum.  Those 
which  join  the  lemniscus  terminate,  first,  in  the  optic 
thalamus,  and,  secondly,  in  the  cortex  as  mentioned 
above  for  the  sensory  system  in  general. 

The  centre  for  the  masticatory  muscles  is  contiguous 
and  anterior  to  the  facial  centre  in  the  cortex. 

The  relationship  of  the  fifth  nerve  to  the  sense  of  taste 
is  important  and  quite  complex  as  shown  in  the  accom- 
panying diagram.     (Fig.  45.) 

A  correct  understanding  of  this  arrangement  is  of 
great  importance  clinically,  since  it  enables  us  to  under- 
stand the  reason  for  the  disturbances  and  occasional 
examples  of  loss  of  taste  in  a  portion  of  one  side  of  the 
tongue  following  middle-ear  disease  through  the  exten- 
sion of  such  disease  process  to  the  Fallopian  canal  trav- 
ersed by  the  chorda  tympani. 

The  Seventh  or  Facial  Nerve. — This  nerve  is  second 
to  none  of  the  cranial  nerves  in  the  importance  of  its 
diagnostic  relations,  and  hence  deserves  careful  con- 
sideration. The  muscles  supplied  by  fibres  from  the 
facial  nerve  are  as  follows:  Occipito-frontalis,  muscles 
of  the  external  ear,  stylo-hyoid,  posterior  belly  of  di- 
gastric, all  of  the  facial  muscles,  platysma,  stapedius, 
tensor  of  palate  and  azygos  uvulae  (possibly). 

The  nerve  takes  a  winding  course  from  its  superficial 
origin  at  the  lower  margin  of  the  pons,  between  the 
olivary  and  restiform  bodies,  to  its  point  of  exit  from  the 
stylo-mastoid  foramen,  passing  through  the  Fallopian 
canal  of  the  temporal  bone.  Within  the  Fallopian  canal 
the  nerve  is  separated  from  the  middle  ear  by  only  a  thin 
lamina  of  bone  pierced  by  foramina  for  a  small  artery. 


THE   NERVOUS   SYSTEM.  63 

the  chorda  tympani  nerve,  and  the  nerve  to  the  stapedius. 
This  fact  is  of  importance,  because  it  explains  how  in- 
flammatory processes  in  the  middle  ear  may  extend  by 
contiguity  to  the  facial  nerve,  with  resulting  paralysis. 

The  angle  or  knee  made  by  the  seventh  nerve  at  the 
hiatus  of  the  bony  canal  is  the  site  of  the  geniculate 
ganglion,  from  which  passes  the  great  superficial  petrosal 
nerve  to  reach  the  spheno-palatine  ganglion  by  way  of 
the  vidian  canal.  The  geniculate  ganglion  is  really  not 
a  ganglion  in  the  ordinary  sense,  but  merely  an  enlarge- 
ment in  the  curve  of  the  nerve-trunk  due  to  the  junction 
of  it  at  that  point  with  several  other  nerves.  The  facial 
and  auditory  nerves  are  very  close  together  at  their 
superficial  origins,  and  are  in  proximity  at  the  internal 
auditory  meatus.  Hence  their  liability  to  suffer  together 
in  lesions  in  this  position.     (See  Fig.  46.) 

The  nucleus  of  the  seventh  nerve  lies  beneath  the 
floor  of  the  fourth  ventricle  at  a  point  ventral  to  the  striae 
medullaris.  It  lies  immediately  dorsal  to  the  medial 
lemniscus  (the  great  sensory  tract)  with  the  superior 
olive  to  its  inner  side  and  the  nucleus  of  the  fifth  lying 
a  little  dorsal  and  to  the  outer  side.  From  this  nucleus 
of  origin  the  fibres  take  a  devious  course,  passing  first  to 
a  point  dorsal  to  the  nucleus  of  the  sixth  nerve,  where 
they  ascend  for  a  short  distance,  finally  making  their  exit 
from  the  medulla  at  the  point  above  mentioned.       (See 

50-) 

There  is  good  reason  for  believing  that  some  of  the 
muscles  supplied  by  fibres  from  the  facial  are  not  repre- 
sented in  the  facial  nucleus,  but  in  the  nuclei  of  other 
nerves.  This  applies  especially  to  the  fibres  composing 
the  superior  branch  of  the  facial  and  which  are  dis- 
tributed to  the  occipito-frontalis,  the  corrugator  supercilii, 
and  the  orbicularis  palpebrarum.    This  group  of  muscles 


64 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


is  not  paralyzed  in  palsies  of  cerebral  origin,  but  only  in 
palsies  involving  the  trunk.  This  can  also  be  explained 
on  the  theory  of  the  bilateral  cortical  representation  of 
these  muscles,  in  favor  of  which  there  is  some  evidence. 


\  INfRAOfiB.S''* 

ORBITAL      f.  /   /AJ  f^J^sf^^  5W- 


MCNTAU  5^ 


FIG.    46. 
Seventh  nerve,  facial,  diagrammatic. 


I.  Great  petrosal,  to  form  vidian  with  No.  5. 
Small  petrosal,  to  otic  ganglion. 
External  petrosal,  to  plexus  on  mid.  meningeal  artery. 

4.  Tympanic  br.  to  stapedius,  etc. 

5.  Br.  from  carotid  plexus,  making  vidian  with  No.  i. 

6.  7.  Brs.  to  auriculo-temporal  of  5th. 
8.   Br.  to  auricular  of  vagus. 

M.  The  ganglion  of  Meckel. 

O.  A.  F.  Orifice  of  aqueductus  Fallopii. 


The  fibres  to  the  orbicularis  palpebrarum  originate  in  the 
nucleus  of  the  third  nerve,  but  course  in  the  seventh. 
The  orbicularis  oris  probably  has  a  certain  representa- 


THE   NERVOUS   SYSTEM.  65 

tion  in  the  hypoglossal  nucleus,  because  of  the  intimate 
association  of  the  movements  of  the  lips  and  the  tongue. 

The  fibres  from  the  facial  nucleus  to  the  cortex  decus- 
sate in  the  pons  just  above  the  nucleus.  Hence,  in  facial 
paralysis  from  a  one-sided  lesion  above  the  middle  of  the 
pons  the  paralysis  of  the  face  is  on  the  side  opposite  to 
the  lesion,  whereas  in  lesions  below  this  level  the  paralysis 
is  on  the  same  side.  The  course  of  the  fibres  through 
the  crus  and  internal  capsule,  and  the  facial  cortical  area 
have  already  been  described. 

The  Eighth  or  Auditory  Nerve. — The  auditory  nerve  is 
formed  by  the  union  of  two  sets  of  fibres  derived  respec- 
tively from  the  cochlea  and  vestibule  and  from  the  semi- 
circular canals.  (See  Figs.  47  and  48.)  These  sets  of  fibres 
differ  in  function,  the  former  conducting  sound-waves, 
and  the  latter  serving  to  carry  from  the  semicircular 
canals  impressions  relative  to  the  movements  and  position 
of  the  body.  Changes  in  bodily  position  probably  cause 
irritation  of  the  mucosa  of  the  semicircular  canals  by 
means  of  solid  bodies  contained  in  the  endolymph. 

Thus  we  are  to  conceive  of  the  vestibular  portion  of 
this  nerve  as  conducting  impressions  relative  to  the  posi- 
tion of  the  body  in  space  and  are  to  consider  the  semi- 
circular canals  of  the  vestibule  as  the  point  from  which 
these  special  sensations  depart.  This  sensory  nerve 
follows  the  same  arrangement  as  obtains  for  sensory 
nerves  in  general.  The  fibres  are  first  interrupted  in  the 
vestibular  ganglion  and  from  this  point  pass  to  enter  the 
medulla  together  with  the  cochlear  fibres  at  a  point  ven- 
tral to  the  corpus  restiformis,  and  to  end  finally  in  the 
vestibular  nucleus  lying  immediately  beneath  the  striae 
medullaris  of  the  floor  of  the  fourth  ventricle.  There 
is  also  a  group  of  larger  cells  lying  to  the  outer  side  of 
this   nucleus,    which  is  commonly   known    as    Deiter's 


66 


DISEASES   OF  THE   NERVOUS   SYSTEM. 


nucleus,  and  these  two  cell  groups  form  the  chief  end- 
ings in  the  medulla  of  the  vestibular  fibres.  There  are 
two  other  nuclei  which  belong  properly  to  the  cerebellum 
which  are  a  part  of  the  vestibular  system  and  in  which 


e.  eU. 


!  // 


9p.  Ci. 


Eighth  or  auditory  nerve,  diagrammatic.  Thin  black  lines,  vestibular  division 
of  eighth  nerve;  dotted  lines,  cochlear  division  of  eighth  nerve;  v.,  vestibule  t 
V.O.,  vestibular  ganglion;  cbl.,  superior  vermis  of  cerebellum  ;  B.,  nucleus  of 
Becterew  ;  d.,  nucleus  of  Deiter  ;  D.Rt,  descending  root  of  eighth  nerve;  t.n., 
triangular  nucleus  ;  v.s.t.,  vestibulo-spinal  tract ;  v. ex.,  vestibulo-cerebellar  tract; 
o.c,  organ  of  Corti  ;  G  c,  ganglion  cochleare  ;  t.ac,  tubercular  acusticum  ;  st.M  , 
striae  medullares ;  ac.n.,  accessory  nucleus:  o  s.,  superior  olive  ;  l.m.,  lateral 
lemniscus  ;  p.q  b.,  posterior  quadrigeminal  body  ;  m.g.b.,  median  geniculate  body 
c.cbi.,  cortex  cerebri,  third  temporal  convolution  ;  C.R.,  corpus  restiforme. 


THE   NERVOUS   SYSTEM.  67 

vestibular  fibres  terminate,  viz.,  the  nucleus  angularis 
and  the  nucleus  tecti.  The  association  of  these  various 
nuclei  with  the  spinal  cord  is  brought  about  by  means 
of  two  systems  of  fibres  which  extend  the  vestibular  ap- 
paratus to  the  lower  levels  of  the  cord.  A  portion  of 
these  fibres  course  in  the  fasciculus  longitudinalis  pos- 
terior and  another  in  the  so-called  descending  acoustic 
root.  It  is  to  be  noted  that  the  latter  really  contains  no 
acoustic  fibres  whatever.  The  cortical  termination  of 
this  system  is  in  the  vermis  of  the  cerebellum.  We  are 
thus  enabled  to  understand  the  occurrence  of  motor  dis- 
turbance in  diseased  conditions  involving  the  middle 
lobe  of  the  cerebellum  on  the  one  hand  or  the  semi- 
circular canals  on  the  other  (Meniere's  disease). 

The  cochlear  fibres  of  the  eighth  nerve  are  those  im- 
mediately concerned  with  the  sense  of  hearing.  Begin- 
ning in  the  mucous  membrane  of  the  cochlea  the  fibres 
are  first  interrupted  in  the  cochlear  ganglion  lying  in  the 
whorl  of  the  cochlea.  The  fibres  proceed,  together  with 
those  from  vestibular  portion  above  described,  to  a  point 
below  the  pons  and  ventral  to  the  corpus  restiformis  to 
enter  the  medulla.  The  primary  distribution  of  these 
fibres  is  twofold;  one  portion  passing  to  the  ventral 
acoustic  nucleus  which  lies  immediately  ventral  to  the 
corpus  restiformis  and  the  other  portion  passing  to  the 
tuberculum  acusticum  (accessory  nucleus)  lying  dorsal 
to  the  corpus  restiformis.  These  two  nuclei  are  the 
primary  medullary  nuclei  of  the  cochlearis.  From  these 
two  nuclei  the  acoustic  tract  is  continued  by  means  of 
fibres  from  the  accessory  nucleus  which  form  the  striae 
acusticae  on  the  floor  of  the  fourth  ventricle  and  cross 
the  middle  line  to  the  opposite  side,  and  fibres  from  the 
chief  nucleus  (ventral),  some  of  which  pass  by  means  of 
the  corpus  trapezoides  to  cross  the  median  line  and  join 


6S  DISEASES   OF   THE   NERVOUS   SYSTEM. 


I'^^r 


The  auditory  tract.  Th,  optic  thalamus;  Int,  int.  capsule;  Ci,  corp.  genicu- 
latum  int.;  Tem,  temporal  lobe  ;  L,  lemniscus  ;  Cqa,  corp.  quadrigeminum  ant.; 
L-qp,  corp.  quad,  post.;  R,  red  nucleus  of  tegmentum  ;  Sn,  substantia  nigra  ;  Ce, 


cochlea  ;  T,  dorsal  nucleus  of  auditory  nerve.     (Starr.) 


THE   NERVOUS   SYSTEM.  69 

the  fibres  from  the  striae  acusticse  and  end  in  the  superior 
oHve  of  the  opposite  side.  From  the  superior  olive  the 
acoustic  tract  is  continued  cerebral-wards  by  means  of 
the  lateral  lemniscus  which  forms  to  the  outer  side  of 
the  superior  olive  to  end  in  the  posterior  quadrigeminal 
body  and  to  be  further  continued  cerebral- wards  as  the 
brachium  of  the  posterior  quadrigeminal  body.  These 
fibres  terminate  in  the  middle  geniculate  body  of  the 
thalamus  opticus  and  are  finally  distributed  to  the  cortex 
of  the  first  temporal  convolution.  The  course  of  the 
auditory  fibres  is  thus  seen  to  be  quite  complex. 

The  wide  difference  in  function  between  the  cochlear 
and  the  vestibular  fibres  of  the  eighth  nerve  should 
always  be  borne  in  mind. 

The  left  cortical  auditory  area  is  especially  related  to 
the  memory  of  words,  its  destruction  producing  the  form 
of  aphasia  known  as  word  deafness. 

The  fact  that  the  eighth  nerve  at  the  base  of  the  brain 
and  at  the  internal  auditory  meatus  lies  side  by  side  with 
the  facial  is  an  anatomical  point  of  some  importance. 

The  Ninth  or  Glosso- Pharyngeal  Nerve. — The  ninth 
nerve  is  distributed  to  the  back  part  of  the  tongue, 
the  soft  palate,  the  upper  part  of  the  pharynx,  and  the 
Eustachian  tube.  Besides  supplying  taste-fibres  to  the 
posterior  part  of  the  tongue  and  motor  fibres  to  the  other 
parts  mentioned,  it  probably  also  furnishes  fibres  of 
common  sensation  to  these  parts  and  to  the  tympanic 
cavity. 

It  has  already  been  stated  that  although  taste-fibres 
are  found  in  the  peripheral  portion  of  this  nerve,  they 
doubtless  ultimately  enter  the  brain  with  the  fifth  nerve. 

Considerable  uncertainty  also  exists  as  to  the  motor 
function  of  the  ninth  nerve.  The  motor  fibres  to  the 
upper  part  of  the  pharynx  come  through  the  pharyngeal 


JO  DISEASES   OF   THE   NERVOUS   SYSTEM. 

plexus,  but  whether  from  the  ninth  or  tenth  nerve  cannot 
be  positively  stated.  The  digastric  branch  of  the  seventh 
communicates  with  the  ninth,  and  it  is  not  improbable 
that  the  stylo- pharyngeus  derives  its  motor  supply  from 
the  former.  Whether  the  ninth  sends  any  motor  fibres 
to  the  palate  has  not  been  determined. 

This  uncertainty  regarding  the  exact  function  of  the 
ninth  nerve  is  due  mainly  to  the  fact  that  in  man  the 
nerve  is  seldom  damaged  by  disease  or  injury  apart  from 
other  adjacent  cranial  nerves,  and  experiments  on  animals 
have  not  been  altogether  satisfactory.  Thus  it  happens 
that  the  functions  of  the  nerve  are  inferred  from  a  study 
of  its  anatomical  distribution — a  method  which  is  apt  to 
be  misleading. 

The  deep  and  superficial  origins  of  the  glosso-pharyn- 
geal  will  be  considered  in  conjunction  with  those  of  the 
tenth  and  eleventh  nerves. 

The  Tenth,  Vagus,  or  Pneumogastric  Nerve. —  This 
nerve  has  the  widest  distribution  of  any  cranial  nerve, 
supplying  as  it  does  the  vocal  and  respiratory  organs, 
the  heart,  most  of  the  alimentary  canal,  and  some  of  the 
abdominal  viscera.  It  has  both  sensory  and  motor 
fibres.  It  sends  sensory  branches  to  the  meninges  along 
the  middle  meningeal  artery,  to  the  posterior  part  of  the 
external  auditory  meatus,  to  the  pharynx,  larynx,  trachea, 
bronchi,  heart,  oesophagus,  stomach,  and  intestines.  Its 
motor  fibres  go  to  the  pharynx  and  larynx.  The  vagus 
is  the  inhibitory  and  accelerator  nerve  of  respiration  and 
the  inhibitory  nerve  of  the  heart.  It  contains  also  motor 
fibres  for  the  oesophagus  and  in  part  for  the  stomach  and 
intestines.  After  receiving  many  fibres  from  the  spinal 
accessory  nerve,  the  pneumogastric  trunk  passes  down 
the  neck  in  the  same  sheath  with  the  carotid  artery.  Its 
pharyngeal  branches  unite  with  those  of  the  ninth  to  form 


THE   NERVOUS   SYSTEM.  71 

the  pharyngeal  plexus.  It  gives  off  the  superior  and 
inferior  (recurrent)  laryngeal  nerves,  which  supply  all 
the  muscles  of  the  larynx.  In  the  abdomen  it  enters 
into  numerous  conjugations  with  the  splanchnic  nerve. 

The  tenth  nerve  emerges  from  the  side  of  the  medulla 
just  anterior  to  the  restiform  body,  as  a  series  of  rootlets, 
the  filaments  of  the  ninth  lying  immediately  above,  and 
the  root  of  the  eleventh  immediately  below.  The  line  of 
separation  between  these  three  nerves  at  their  superficial 
origin  is  not  sharply  defined,  and  hence  it  is  rare  for  any 
lesion  at  this  point,  even  though  small,  to  affect  one  of 
these  nerves  alone. 

A  part  of  the  Eleventh  or  Spinal  Accessory  Nerve  joins 
the  pneumogastric,  and  receives  its  title  because  of  being 
accessory  to  the  vagus.  The  filaments  which  arise  in 
this  close  relation  to  the  tenth  nerve  constitute  the  acces- 
sory portion,  the  spinal  portion  arising  at  a  wide  interval 
from  a  lower  level,  in  the  anterior  horn  of  the  spinal 
cord. 

The  central  origin  of  the  ninth,  tenth,  and  eleventh 
nerves  is  from  a  continuous  series  of  cell-nests  forming 
a  longitudinal,  narrow,  gray  column,  which  lies  just 
lateral  to  the  eminentia  teres  of  the  fourth  ventricle,  with 
its  long  axis  running  downward  from  the  level  of  the 
auditory  nucleus  above. 

Some  of  the  upper  cells  of  this  column  give  origin  to 
the  ninth,  the  middle  cells  to  the  tenth,  and  the  lowest 
cells  to  the  accessory  portion  of  the  eleventh  nerve. 
Motor  fibres  are  derived  from  a  special  group  of  cells 
known  as  the  nucleus  ambiguous.  From  these  groups 
of  cells  the  fibres  run  outward  through  the  formatio 
reticularis  of  the  medulla  to  their  superficial  origins  as 
described.  In  passing  through  the  medulla  these  bundles 
of  fibres  traverse  the  ascending  root  of  the  fifth  nerve. 


T^ 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


ru)OR  or  rouRTH  vcnthicle 


and   this  fact  furnishes  an  anatomical   explanation   for 
some  of  the  reflex  relations  of  the  fifth  nerve. 

The  spinal  portion  of  the  eleventh  nerve  rises  from  the 
upper  cervical  portion  of  the  spinal  cord,  by  a  series  of 
filaments  from  the  anterior  horn,  and  then  takes  a  unique 
course  upwards  into  the  cranial  cavity  to  join  tempo- 
rarily the  accessory  portion  before  again  passing  out  of 

the  cranial  cavity  to 
supply  the  trapezius 
and  sterno  -  cleido- 
mastoid  with  motor 
fibres.  It  supplies 
these  two  muscles  in 
conjunction  with 
branches  from  some 
of  the  cervical 
nerves  proper. 

The  Twelfth  or 
Hypoglossal  Nerve. 
— This  is  a  purely 
motor  nerve  des- 
tined for  the  mus- 
cles of  the  tongue 
and  for  most  of  the 
muscles  connected 
with  the  hyoid  bone. 
It  arises  from  the 
medulla  between  the  anterior  pyramid  and  olivary  body, 
by  a  series  of  filaments  which  are  in  line  with  the  motor 
roots  of  the  spinal  nerves  and  immediately  adjacent  to 
the  rootlets  of  the  eleventh.  The  twelfth  pair  are  sepa- 
rated at  their  superficial  origin  by  the  prominent  an- 
terior pyramids,  and  are  rarely  involved  together  by 
disease    external    to    the    medulla.      The    eleventh    and 


FIG.  49. 

Diagram  of  a  transverse  section  through  ^  the 
medulla  at  the  lower  level  of  the  fourth  ventricle. 
Especially  to  be  noted  are  the  tenth  and  twelfth 
nerves  and  their  nuclei  of  origin,  the  position  of  the 
olivary  nucleus,  the  fillet,  the  anterior  pyramids  (the 
motor  path),  the  restiform  body,  and  the  ascending 
root  of  the  fifth  nerve.  Between  the  olive  in  front 
and  the  tenth  and  twellth  nuclei  behind  lies  the 
substantia  reticularis  (the  path  of  common  sensi- 
bility). The  posterior  longitudinal  bundles  lie  on 
either  side  of  the  median  line  between  the  twelfth 
nerves. 


THE   NERVOUS   SYSTEM. 


n 


twelfth    are   so    closely   associated   at   their  origin   that 

they  are  frequently  involved  together,  the  result  being 

paralysis  of  the  tongue  and  vocal  cord  of  the  same  side. 

The  nucleus  of  the  hypoglossal  nerve  is  a  long  column 


FIG.  50. 

Schematic  basal  section  of  the  medulla  oblongata,  Po,  pons;  Brcj,  Brachium 
conjunctivum ;  Va,  spinal,  Vd,  cerebral,  Vm,  motor,  Vs,  sensory  root  of  the 
trigeminal  nerve  ;  NVm,  motor,  NVs,  sensory  root  of  the  trigeminal  nucleus  ; 
NVII,  nucleus  of  the  facial  nerve  ;  VII,  a,  b,  c,  root  of  the  facial  nerve  ;  VII, 
exit  of  the  facial  nerve;  NVI,  abducens  nucleus;  NXII,  hypoglossal  nucleus; 
IXa,  spinal  root  of  the  glosso-pharyngeal  nerve  (X)  ;  IX,  its  exit ;  No,  olivary 
nucleus;  X,  vagus  nerve  ^or  glosso-pharyngeal)  showing  its  part  origin  from  the 
nucleus  ambiguous  ;  Na,  nucleus  ambiguous  ;  Ca,  anterior  horn  of  the  spinal  cord; 
Ca,  Na,  NVII,  NVm,  column  of  origin  of  motor  nuclei. 


of  motor  nerve-cells  extending  from  the  level  of  the  lower 
angle  of  the  fourth  ventricle  (calamus  scriptorius)  down- 
ward to  the  decussation  of  the  pyramids.  It  lies  close 
to  the  median  line,  and  in  part  of  its  course  just  medial 


74  DISEASES   OF   THE   NERVOUS   SYSTEM. 

to  the  spinal-accessory  nucleus.  To  reach  the  surface 
of  the  medulla,  the  fibres  pass  from  the  nucleus  forward 
and  outwards,  through  the  formatio  reticularis  and  be- 
tween the  olivary  nucleus  and  the  anterior  pyramid,  some 
of  the  fibres  generally  traversing  the  former.  The  rela- 
tive origin  and  course  of  the  ninth,  tenth,  and  twelfth 
nerves  in  the  medulla  are  shown  in  the  schematic  dia- 
gram of  Fig.  50. 

The  Meninges  of  the  Brain  and  Cord. — There 
are  three  membranes  which  enclose  the  central  nervous 
system.  The  outer  or  dura  mater  is  the  thickest.  It  is 
formed  of  dense  fibrous  tissue,  and  in  the  vertebral  canal 
is  separated  from  the  bony  walls  by  a  layer  of  fat  and  a 
plexus  of  large  veins,  while  in  the  cranium  it  is  closely 
approximate  to  the  bones.  The  spinal  dura  is  thus  a 
loosely  suspended  long  sac,  attached  only  slightly  to  the 
spinal  canal  on  its  anterior  surface.  This  outer  space  in 
the  spine  is  called  the  epidural  space,  and  is  not  con- 
nected with  an  analogous  space  in  the  skull.  The  dura 
has  comparatively  few  blood-vessels,  but  is  well  supplied 
with  lymphatics  and  with  sensory  nerves  (in  the  skull 
by  the  fifth  and  ninth  nerves,  in  the  spine  by  filaments 
from  the  posterior  roots).  The  inner  surface  is  lined  by 
endothelium  and  encloses  the  lymphatic  subdural  space, 
which  contains  a  variable  amount  of  serum.  The  middle 
membrane  is  the  arachnoid,  delicate  and  with  few  blood- 
vessels and  no  nerves,  enclosing  what  is  known  as  the 
lymphatic  subarachnoid  space.  It  is  lined  with  endothe- 
lium on  both  surfaces.  On  the  brain  the  arachnoid  is 
separated  from  the  innermost  membrane  or  pia  mater, 
between  the  convolutions,  where  the  latter  dips  down 
into  the  sulci;  but  the  separation  between  the  two  is 
complete  in  the  spinal  canal.  There  is  no  direct  com- 
munication   between    the    subdural    and   subarachnoid 


THE   NERVOUS   SYSTEM.  75 

lymph-spaces,  but  there  is  a  free  communication  be- 
tween the  ventricles  of  the  brain  and  the  latter  space  by- 
means  of  the  foramen  of  Magendie  and  two  smaller 
foramina  in  a  part  of  the  membrane  projecting  dorsally 
into  the  fourth  ventricle.  The  base  of  the  brain,  there- 
fore, lies  upon  a  sort  of  water-bed,  being  separated  from 
the  base  of  the  skull  by  an  interval  occupied  by  sub- 
arachnoid fluid  and  trabeculae.  The  nerve-roots  and 
basal  blood-vessels  are  thus  carefully  protected  from 
certain  forms  of  injury. 

The  pia  mater  is  a  delicate  membrane  extremely  rich 
in  blood-vessels,  lymphatics,  and  vasomotor  nerves.  It 
dips  down  between  the  convolutions  of  the  brain,  and 
sends  connective-tissue  septa  into  the  cord.  The  blood- 
vessels and  nerves  pass  inward  from  this  membrane  to 
the  central  nervous  system,  while  the  lymphatics  com- 
municate externally  with  the  subarachnoid  space. 

The  whitish  granulations,  known  as  Pacchionian 
bodies,  which  are  seen  upon  the  surface  of  the  mem- 
branes on  each  side  of  the  median  line  of  the  vertex  of 
the  brain,  are  connective-tissue  villi  which  subserve  the 
outflow  of  cerebro-spinal  fluid  from  the  subdural  and 
subarachnoid  spaces  into  the  longitudinal  and  other 
dural  sinuses. 

The  Blood-Supply  of  the  Spinal  Cord  and 
Brain. — Branches  from  the  vertebral,  intercostal,  and 
other  arteries  enter  the  spinal  canal  with  the  spinal 
nerves.  Anterior  branches  pass  along  the  anterior 
nerve-roots  to  the  anterior  median  fissure,  where  they 
join  to  form  a  continuous  vertical  vessel — the  anterior 
spinal  artery.  Branches  pass  to  the  bottom  of  the  fissure 
and  enter  the  cord,  dividing  into  lateral  twigs  at  the 
anterior  commissure,  which  are  destined  for  the  anterior 
horn  and  partly  for  the  lateral  column.     Ramifications 


']6  DISEASES   OF   THE   NERVOUS   SYSTEM. 

are  made  by  both  the  anterior  and  posterior  arteries  in 
the  pia  mater,  and  twigs  are  given  off  everywhere  to  the 
white  substance  of  the  cord  along  the  connective-tissue 
septa.  The  posterior  arteries  send  branches  into  the 
caput  cornu  posterioris  where  they  take  vertical  courses. 

The  veins  have  a  very  similar  arrangement.  Combin- 
ing to  form  anterior  and  posterior  spinal  veins,  these 
empty  their  blood  into  the  large  venous  plexuses  of  the 
epidural  space.  These  plexuses  receive  blood  also  from 
the  vertebrae  and  even  from  the  skin  and  subcutaneous 
structures  of  the  back,  finally  delivering  it  to  the  verte- 
bral and  intercostal  veins.  The  tortuous  course  of  the 
arteries  destined  for  the  spinal  cord  and  the  large  size 
of  the  venous  plexuses  undoubtedly  protect  those  por- 
tions of  the  central  nervous  system  from  the  dangers  of 
high  pressure,  over-distension,  and  rupture. 

The  blood-supply  of  the  brain  is  of  far  greater  practical 
importance  to  the  physician  than  that  of  the  spinal  cord. 
It  is  derived  from  the  carotid  and  vertebral  arteries. 
The  courses  of  the  left  carotid  and  of  the  left  vertebral 
are  much  nearer  a  direct  line  from  the  heart  than  those 
of  their  companions  of  the  opposite  side,  a  fact  which 
renders  them  more  liable  to  receive  embolic  plugs 
washed  away  from  the  endocardium. 

On  each  side  the  internal  carotid  divides  into  the  an- 
terior and  middle  cerebral  arteries,  while  the  basilar 
artery,  formed  by  the  two  vertebrals,  redivides  into  the 
two  posterior  cerebral  arteries.  These  three  arteries, 
the  anterior,  middle,  and  posterior  cerebral,  supply  each 
hemisphere  in  the  region  designated  by  their  name. 
Practically  the  middle  cerebral  or  Sylvian  artery  is 
of  especial  importance,  for,  coursing  through  the  fis- 
sure of  Sylvius,  it  is  distributed  over  the  motor  area 
of   the  cortex.     Hence    the    hemiplegia   so    often   pro* 


THE   NERVOUS   SYSTEM. 


17 


duced  by  embolism  and  by  thrombosis  of  this  artery. 
Although  it  has   anastomoses   with  branches   from   the 


FIG.  51. 

Arteries  at  the  base  of  the  brain.      (Oppenheim.) 

other  arteries  on  the  surface  of  the  brain,  they  are  rarely 
sufficient  for  the  establishment  of  a  collateral  circulation. 


78  DISEASES   OF   THE   NERVOUS   SYSTEM. 

The  branches  sent  by  these  superficial  vessels  are  short 
ones  for  the  cortex,  and  long  ones  for  the  white  matter. 
They  enter  straight  into  the  cerebral  substance  from  the 
pia  and  have  very  little  communication  with  each  other, 
and  none  with  the  vessels  entering  the  base  of  the  brain 
from  the  circle  of  Willis. 

The  central  arteries  are  those  given  off  from  the  circle 
of  Willis  and  from  the  first  part  of  the  trunks  of  the  three 
cerebral  arteries,  and  furnish  the  blood-supply  for  the 
basal  ganglia  and  adjacent  white  substance.  These  ves- 
sels have  no  anastomoses  within  the  brain.  The  most 
important  of  the  central  arteries  is  the  group  given  off 
within  the  first  inch  of  the  trunk  of  the  middle  cerebral 
artery,  and  known  as  the  "  lateral  group."  They  come 
off  at  a  right  angle  from  the  main  artery,  and  entering 
the  anterior  perforated  space,  just  in  front  of  the  optic 
tract  and  behind  the  roots  of  the  olfactory  nerve,  are 
distributed  to  part  of  the  caudate  nucleus,  to  the  lentic- 
ular nucleus,  the  internal  capsule,  and  to  part  of  the 
optic  thalamus.  The  anterior  vessels  of  this  group  are 
sometimes  called  the  lenticulo-striate  and  the  posterior 
the  lenticulo-thalamic  arteries.  It  is  one  of  these  vessels 
which  is  so  liable  to  rupture  and  produce  the  serious 
symptoms  accompanying  cerebral  hemorrhage. 

The  pons,  medulla,  and  cerebellum  derive  their  arteries 
from  the  vertebrals  and  basilar.  The  veins  from  the 
outer  and  median  surfaces  of  the  hemispheres  course 
upwards  to  enter  the  superior  longitudinal  sinus,  while 
those  from  the  base  of  the  brajn  empty  into  the  cavern- 
ous, petrosal,  and  lateral  sinuses.  The  veins  of  Galen, 
carrying  blood  from  the  choroid  plexuses  and  walls  of 
the  ventricles  and  from  the  upper  surface  of  the  cerebel- 
lum, terminate  in  the  straight  sinus.  There  are  free 
anastomoses  between  all  of  the  sinuses,   and  there  are 


THE   NERVOUS   SYSTEM. 


79 


FIG.  52. 

Area  of  cortex  supplied  by  the 
branches  of  the  middle  cerebral 
artery. 


FIG.  53. 

Area  of  cortex  on  outer  surface  of 
hemisphere  supplied  by  the  anterior 
cerebral  artery. 


FIG.  54. 

Area  of  cortex  on  inner  surface  of 
hemisphere  supplied  by  the  anterior 
cerebral  artery.  The  dotted  lines 
separate  areas  supplied  by  different 
branches  of  the  artery. 


FIG.  55. 

Area  of  cortex  on  the  outer  surface 
of  the  hemisphere  supplied  by  the 
posterior  cerebral  artery. 


FIG.  56. 

Area  of  cortex  on  the  inner  surface  of 
the  hemisphere  supplied  by  the  posterior 
cerebral  artery.  The  dotted  lines  sepa- 
rate areas  supplied  by  different  branches 
of  the  artery 


So 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


also  communications  between  them  and  veins  outside 
the  cranial  cavity.  Thus,  the  ophthalmic  vein  enters 
the  cavernous  sinus;  veins  from  the  nose  pass  into  the 
superior  longitudinal;  veins  from  the  diploe  of  the  skull 
communicate  freely  with  various  sinuses;  some  of  the 
mastoid  veins  open  into  the  lateral  sinus;  veins  from 
the  internal  ear  reach  the  superior  petrosal  sinus;  and 
there  are  even  numerous  communications,  some  direct, 
others  indirect,  between  veins  of  the  face,  scalp,  and 
neck  and  the  cerebral  sinuses.     The  spinal  venous  sys- 


FiG.  57. 

Diagram  of  the  blood  supply  of  the  central  ganglia  and  internal  capsu! 
C,  middle  cerebral  artery;  E  E,  external,  I,  internal,  lenticulo-striate 
III  V,  third  ventricle.     (After  Duret.) 


e.     Mid. 
arteries : 


tern  is  connected  with  that  of  the  brain  by  six  veins. 
The  cerebral  veins  and  sinuses  have  no  valves. 

Cranio  -  Cerebral  Topography.  Spinal  and 
Spinal-Cord  Topography. — A  knowledge  of  some 
of  the  relations  of  certain  parts  of  the  surface  of  the 
brain  to  the  skull  is  of  practical  importance  in  diagnosis 
and  for  surgical  purposes.  The  diagram  on  page  83 
illustrates  sufficiently  well  the  general  correspondence  be- 
tween the  chief  convolutions  and  fissures  and  the  cranial 
bones.     It  will  be  noted  that  under  the  frontal  bone  lie 


THE  NERVOUS   SYSTEM. 


8l 


three  fourths  of  the  first  frontal  convolution,  about  five 
sixths  of  the  second,  and  nearly  all  of  the  third  frontal 
convolution.  Under  the  temporal  bone  lies  all  of  the 
temporal  lobe,  except  its  most  anterior  and  its  most  pos- 
terior portion.  Under  the  occipital  bone  lies  about  one 
half  (posterior)  of  the  occipital  lobe.  The  parietal  bone 
covers  what  remains  of  the  cortex. 

The  fissure  of  Rolando  is  the  part  of  the  brain  which 
it  is  the  most  often  necessary  to  locate.  The  upper  end 
of  the  fissure  is  best 
found  by  measuring 
the  distance  from 
the  root  of  the  nose 
(glabella)  to  the  ex- 
ternal occipital  pro- 
tuberance (i  n  i  o  n) 
along  the  middle 
line.  A  point  one 
half  inch  posterior 
to  the  middle  point 
of  this  distance 
marks  the  upper  ex- 
tremity of  the  fis- 
sure. The  fissure  of  Rolando  in  its  upper  two  thirds 
makes  an  angle  of  sixty-seven  degrees  with  the  median 
line,  in  its  lower  one  third  the  fissure  is  a  little  more  ver- 
tical. The  average  length  of  the  fissure  is  about  three 
and  a  half  inches.  The  central  convolutions  occupy 
about  an  inch  anterior  and  posterior  to  the  fissure,  and 
the  positions  of  the  leg  and  face  centres  may  thus  be 
approximately  located. 

What  is  known  as  the  Sylvian  line  extends  from  the 
external  angular  process  of  the  frontal  bone  to  a  point 
three  quarters  of  an  inch  below  the  most  prominent  part 


FIG.    58. 

Diagram  showing  the  relation  of  the  convolutions 
to  the  skull. 


82 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


The  mutual  relations  of  the  vertebral 
bodies  and  spines  to  the  segments  of  the 
cord  and  to  the  exit  of  the  nerves  (Gowers). 


of  the  parietal  boss.  The 
posterior  limb  of  the  fis- 
sure of  Sylvius  lies  under 
the  posterior  three  fifths 
of  this  line.  The  anterior 
limb  of  the  fissure  of 
Sylvius  ascends  almost 
vertically  from  the  syl- 
vian line  at  the  middle  of 
the  zygoma.  A  continu- 
ation of  the  Sylvian  line 
backwards  to  the  sagittal 
suture  marks  the  position 
of  the  parieto- occipital 
fissure. 

A  knowledge  of  the  re- 
lations of  the  various  seg- 
ments of  the  spinal  cord 
to  the  spines  of  the  ver- 
tebrae is  essential  both  for 
the  diagnosis  and  success- 
ful treatment  of  certain 
spinal-cord  a  ff  ec  t  i  o  n  s. 
Theserelations  varysome- 
what  in  different  individ- 
uals, but  one  description 
is  sufficiently  accurate  for 
practical  purposes.  The 
chief  facts  may  be  de- 
duced from  the  accom- 
panying drawing.  These 
facts  are  as  follows: 

(i)  The  spinal  cord  in 
the    adult    terminates    at 


THE   NERVOUS    SYSTEM.  83 

about  the  lower  border  of  the  first  lumbar  vertebra  (in 
children  one  to  two  years  of  age  the  cord  extends  as  low 
as  the  third  or  fourth  lumbar  vertebra). 

(2)  The  different  pairs  of  nerves,  excepting  the  upper 
cervical  nerves,  leave  the  vertebrae  from  which  they  are 
named  at  a  lower  level  than  that  at  which  they  are  given 
off  from  the  corresponding  segments  of  the  cord.  This 
difference  in  the  level  of  exit  and  origin  of  the  nerve- 
roots  increases  from  above  downwards/  The  first, 
second,  and  third  cervical  spines  correspond  in  level  to 
the  origins  from  the  cord  of  the  third,  fourth,  and  fifth 
cervical  nerves.  Between  the  fourth  and  fifth  spines 
arises  the  sixth  pair;  between  the  fifth  and  sixth,  the 
seventh  cervical  pair.  The  seventh  cervical  spine  is 
opposite  the  first  dorsal  segment.  The  fifth,  sixth, 
seventh,  eighth,  ninth,  and  tenth  spines  correspond 
nearly  to  the  seventh,  eighth,  ninth,  tenth,  eleventh, 
and  twelfth  nerve-roots  and  spinal  segments.  The  first 
lumbar  nerve  arises  opposite  the  eleventh  dorsal  spine. 
The  first  sacral  nerve  arises  just  above  the  first  lumbar 
spine. 

(3)  The  cervical  enlargement  of  the  cord  corresponds 
very  closely  to  the  cervical  spines.  The  lumbar  enlarge- 
ment corresponds  to  the  tenth,  eleventh,  and  twelfth 
dorsal  and  to  the  first  lumbar  spines. 

^  It  is  convenient  at  times  to  know  the  exact  lengths  of  certain  of 
these  nerves  (especially  the  lower  ones)  between  their  origin  and  their 
exit  from  the  spinal  canal.  It  is  easy  to  remember  that  the  course  of 
the  third  lumbar  is  about  three  inches,  and  that  of  the  fifth  lumbar 
about  five  inches. 


CHAPTER    II. 

THE    SYMPTOMATOLOGY    OF    NERVOUS    DISEASES. 

The  symptoms  of  organic  disease  of  the  nervous  sys- 
tem, though  exceedingly  varied,  can  for  the  most  part  be 
referred  to  the  operation  of  a  small  number  of  funda- 
mental mechanisms.  In  the  first  place  an  important  class 
of  symptoms  result  from  the  destruction,  complete  or  in- 
complete, of  nervous  structures. 

Complete  destruction  of  a  portion  of  the  nervous  sys- 
tem always  results  in  complete  loss  of  function  of  the 
part  involved.  This  loss  of  function  is  permanent  except 
in  cases  where  neighboring  parts  of  the  nervous  system 
make  up  the  loss,  to  some  extent,  by  compensation.  In 
adults  extensive  compensation  can  occur  only  in  the  brain, 
some  functions  of  which  are  diffuse — that  is,  dependent  on 
the  activity  of  a  large  number  of  cells  scattered  over  a 
wide  area.  Thus  a  destructive  lesion  in  the  frontal  lobe 
of  the  brain,  which  is  chiefly  concerned  with  higher  intel- 
lectual processes,  does  not  cause  any  special  loss  of  func- 
tion, but  simply  a  general  lowering  of  its  functional 
activity  as  a  whole.  The  restoration  of  speech  which 
occurs  in  children  in  whom  the  motor  speech  centre  of 
the  left  side  has  been  destroyed,  is  a  good  example  of 
compensation,  which,  in  this  instance,  occurs  in  corre- 
sponding structures  of  the  opposite  hemisphere.  Com- 
pensation is  limited,  where,  as  in  the  cord  and  the  medulla, 
and  some  parts  of  the  brain,  a  particular  function  is  per- 

b4 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      85 

formed  only  by  certain   sharply  limited  structures,  and 
these  are  destroyed. 

Partial  damage  of  nerve  elements  also  gives  rise  to  loss 
of  function,  which  may  be  of  any  degree  of  severity. 
The  following  are  the  chief  causes  of  structural  damage 
to  nerve  elements  : 

1.  Mechanical  Injury. — Mechanical  damage  may 
cause  destruction  of  cells  and  fibres,  or  interruptions  in 
their  continuity.  Hemorrhage  or  trauma  are  the  chief 
causes  of  such  mechanical  lesions.  There  is  absolute 
loss  of  function  of  the  parts  thus  injured. 

An  important  form  of  mechanical  injury  to  nervous 
structures  is  pressure.  The  severity  of  the  effects  of 
pressure  depend  largely  on  the  rapidity  of  its  production. 
A  considerable  degree  of  pressure,  if  of  very  gradual 
development,  may  give  rise  to  little  functional  disturb- 
ance. Thus  the  entire  motor  area  of  the  brain  may  be 
gently  compressed  by  slow  subdural  or  subarachnoid 
hemorrhage  without  giving  rise  to  motor  paralysis. 
Again,  the  spinal  cord  may  be  slowly  compressed  by 
Pott's  disease  to  a  surprising  degree  with  little  or  no 
interference  with  the  functions  of  the  cord.  A  slight 
grade  of  pressure,  on  the  contrary,  if  rapidly  brought 
about,  does  far  more  damage  to  the  nerve  elements,  and 
may  cause  immediate  loss  of  function. 

2.  Loss  of  Blood  Supply,  Partial  or  Complete. — 
The  loss  of  function  is  complete,  if  the  blood  supply  is 
arrested  ;  partial,  if  there  is  merely  diminution  in  blood 
supply.  In  both  cases  the  effect  comes  on  very  rapidly 
if  the  interference  with  the  circulation  be  sudden. 
Where  the  interference  is  gradual,  the  effects  are  of  more 
gradual  onset  and  of  less  severity,  probably  because  there 
is  time  for  the  establishment  of  a  collateral  circulation. 

Both  cells  and  fibres  suffer  from  diminished  blood  sup- 


so  DISEASES   OF   THE   NERVOUS   SYSTEM. 

ply,  but  not  equally.  The  nerve-cells  are  in  general  far 
more  sensitive  to  the  effects  of  deficient  blood  supply. 
For  example,  if  the  blood  supply  to  the  spinal  cord 
of  the  rabbit  be  cut  off  by  compression  of  the  abdomi- 
nal aorta,  the  motor  ganglion-cells  cease  to  functionate  at 
once,  but  the  white  matter  shows  no  reaction  at  first.  If 
the  circulation  is  restored  after  half  an  hour,  the  cells 
recover  function  :  if  not,  necrotic  changes  begin,  first  in 
the  cells,  later  in  the  white  matter. 

3.  Inflammation,  which  involves  the  nerve  and  fibres 
(parenchyma),  the  blood-vessels,  and  usually  the  intersti- 
tial tissue.  The  process  may  be  acute  or  chronic  ;  in  the 
latter  case  the  changes  begin  in  interstitial  structures,  and 
secondarily  damage  the  nervous  elements. 

4.  Wasting  of  Nerve  Elements. — A  very  frequent 
cause  of  the  destruction  of  nervous  tissues  is  the  degen- 
eration which  affects  cells  and  fibres.  Often  degenerative 
changes  occur  in  these  structures  as  a  consequence  of 
inflammation  of  interstitial  tissues,  but  in  a  large  and  im- 
portant class  of  cases  the  changes  in  the  cells  and  fibres 
are  primary.  Many  symptoms  however  of  nervous  disease, 
result  not  from  destruction  of  nerve  elements  but  from 
their  irritation.  This  irritation  usually  expresses  itself  by 
an  increase  of  action,  or  functional  overaction,  as,  for 
example,  in  convulsive  movements,  or  hyperaesthesia. 

But  irritation  does  not  always  result  in  overaction  ;  it 
may  lessen  function  by  the  process  termed  inhibition. 
A  good  example  of  this  effect  of  irritative  inhibition  is 
the  loss  of  the  knee-jerk  which  follows  immediately  on  a 
severe  mechanical  injury  to  the  spinal  cord  above  the 
lumbar  enlargement,  say  in  the  cervical  region.  The 
important  difference  between  the  diminution  or  loss  of 
function  which  results  from  irritative  inhibition  and  that 
which  results  from  a  destructive  lesion,  is  that  the  former 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.       87 

is  temporary,  the  latter  permanent.  It  is  important  to 
remember  that  the  effects  of  destruction  and  those  ot 
irritation  are  often  met  with  in  combination,  as  for  ex- 
ample when  a  tumor  causes  both  paralysis  and  spasm. 

The  mechanisms  which  have  been  mentioned  as  pro- 
ductive of  symptoms  relate  mainly  to  organic  diseases. 
There  is  a  large  and  important  class  of  symptoms  which 
cannot  be  referred  to  structural  changes  in  the  nervous 
elements  but  which  probably  depend  upon  changes  in 
their  nutrition,  changes  of  whose  nature  we  at  present 
know  little. 

Motor  Paralysis.  —  Loss  of  voluntary  muscular 
power  (paralysis)  may  result  from  disease  involving  any 
part  of  the  motor  path — its  upper  segriient  or  its  lower 
segment  (p.  24).  Thus,  paralysis  may  arise  from  dis- 
ease of  the  motor  cortex,  of  the  motor  path  in  the  cen- 
trum semiovale,  internal  capsule,  crus,  pons,  medulla,  or 
cord  (upper  segment),  or  from  disease  of  the  anterior 
cornual  cells,  anterior  nerve-roots,  motor  nerves,  or  mus- 
cle plates  (lower  segment). 

Disease  in  other  parts  of  the  nervous  system  than 
those  enumerated  does  not  cause  motor  paralysis,  unless 
it  does  so  by  giving  rise  to  pressure  on  these  structures. 

Paralysis  may  or  may  not  be  associated  with  wasting 
or  atrophy  of  the  muscles  paralyzed,  according  to  the 
position  of  the  lesion. 

In  general  it  may  be  said  that  paralysis  and  marked 
atrophy  are  rarely  'associated  in  disease  involving  the 
cerebro-spinal  or  upper  segment  of  the  motor  path 
(p.  24),  and  that  they  are  nearly  always  associated  in 
disease  of  any  part,  of  the  lower  segment  (ganglion-cells, 
nerve-roots,  or  nerves). 

The  varieties  of  paralysis  according  to  distribution 
are   without    number,   but  certain  typical    forms  are  of 


88 


DISEASES   OF  THE   NERVOUS   SYSTEM. 


x-'^C 


Diagram  showing  the  effect  of  lesions  at  different  levels  of  the  motor  path.  A 
small  lesion  at  some  point,  A,  between  the  cortex  aud  the  internal  capsule,  will 
cause  a  local  paralysis — a  lesion  at  A  would  cause  a  brachial  monoplegia;  a  lesion 
at  B  will  produce  hemiplegia  (complete)  on  the  side  opposite  the  lesion  ;  a  lesion 
at  C  would  cause  paralysis  of  the  Hid  nerve  on  l\\&same  side,  and  of  the  face.  arm. 
and  leg  on  the  opposite  side ;  a  lesion  at  D  would  cause  hemiplegia  on  the  opposite 
side  ;  a  lesion  at  E  would  cause  paralysis  of  the  face  on  the  same  side,  of  the  arm 
and  leg  on  the  opposite  side;  a  lesion  at  F,  paralysis  of  arm  and  leg  on  the 
opposite  side  (and  perhaps  of  the  XI  1th  nerve  on  the  same  side— Xllth  nerve 
not  represented)  ;  a  lesion  at  G  would  cause  paralysis  of  the  arm  and  leg  on  the 
same  side. 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.        89 

practical  importance  from  their  diagnostic  significance 
and  frequent  occurrence. 

Hemiplegia. — Hemiplegia  is  the  paralysis  of  several 
groups  of  muscles  of  one  lateral  half  of  the  body.  In 
its  more  common  form  there  is  a  more  or  less  marked 
loss  of  voluntary  motion  involving  face,  tongue,  arm, 
and  leg  on  the  same  side — complete  hemiplegia.  Such 
hemiplegia  may  result  from  a  lesion  anywhere  in  the  motor 
tract  between  the  cortex  and  the  pons.  In  the  pons  and 
crus  the  fibres  of  the  motor  tract  are  so  close  together 
that  a  lesion  practically  always  involves  all  the  fibres  of 
the  tract,  and  complete  hemiplegia  results.  In  the  inter- 
nal capsule  the  fibres  begin  to  spread  out,  and  a  lesion 
here,  if  very  small,  may  fail  to  involve  all  its  fibres,'  thus 
giving  rise  to  an  incomplete  hemiplegia.  While  this  is 
theoretically  possible  it  is  practically  of  rare  occurrence, 
and  a  more  or  less  complete  hemiplegia  in  range  is  the 
rule.  The  motor  fibres  are  more  and  more  widely  sepa- 
rated in  their  course  through  the  corona  radiata  of  the 
cortex.  Hence,  in  these  situations  even  a  lesion  of  con- 
siderable size  may  fail  to  affect  all  the  parts  of  one  side, 
face,  tongue,  arm,  and  leg.  Thus  it  is  not  rare  for  the 
face  and  leg  to  escape  more  or  less  completely,  the  arm 
being  paralyzed  alone.  Such  a  paralysis  is  called  brachial 
monoplegia.  Other  monoplegias,  as  face  and  arm,  arm 
and  leg,  but  not  face  and  leg,  may  occur  from  single 
lesions. 

The  expression  "complete  hemiplegia"  implies  that  the 
paralysis  affects  all  of  one  side,  but  this  is  not  strictly 
true.  Thus  the  upper  facial  muscles  (orbicularis  pal- 
pebrarum and  occipito-frontalis)  move  almost  or  quite  as 
well  as  on  the  non-paralyzed  side,  and  the  muscles  of 
the  eyeball  and  the  muscles  of  mastication  are  unaffected. 
The  tongue  as  a  whole  deviates  towards  the  paralyzed 


90 


DISEASES   OF  THE  NERVOUS   SYSTEM. 


side  when  protruded  because  the  projecting  apparatus 
on  that  side  is  weakened  and  does  not  oppose  the  genio- 
hyo-glossus.  Inasmuch  as  this  muscle  also  retracts  as 
well  as  protrudes  the  tongue,  the  organ  is  not  so  high  on 
the  paralyzed  side  when  in  repose.  The  muscles  of 
respiration  and  the  muscles  of  the  face  and  trunk  are 
not  involved  in  ordinary  action.  The  movements  of 
the  superior  intercostal  muscles  are  greater  on  the 
paralyzed  side,  though  if  the  patient  take  a  deep  respira- 
tion there  is  defective  chest  expansion  of  the  affected 
side. 

In  general  it  may  be  said  that  in  hemiplegia  the  extent 


FIG.   6l. 


Respiratory  movements  in  a  case  of  right  hemiplegia.     R,  right  side  ;  L,  left 
ie  ;  A  B  and  a'  b',  normal  respiration  ;  b  c  and  b'  c',  forced  respiration. 


sid 


of  the  paralysis  in  the  part  is  proportional  to  the  degree 
in  which  the  part  is  capable  of  unilateral  use.  Thus 
the  muscles  of  one  hand  are  habitually  employed  alone, 
are  chiefly  innervated  from  one  side  of  the  brain,  and 
suffer  severely,  while  the  intercostals  of  one  side  are 
never  used  by  themselves,  are  innervated  from  both 
hemispheres,  although  not  quite  equally.  The  leg, 
which,  though  generally  used  with  its  fellow,  is  capa- 
ble of  some  unilateral  use  and  is  also  represented 
to  some  extent  in  both  hemispheres,  suffers  less,  and 
usually  recovers  more  power  than  the  arm.  This  re- 
covery is  through   compensation   by   the  normal   hemi- 


SYMPTOMATOLOGY   OF  NERVOUS   DISEASES.        9I 

sphere,  whose  nerve  impulses  probably  travel  over 
other  than  pyramidal  tracts.  In  early  life  the  amount 
of  recovery  is  usually  extensive.  Recovery  is  more 
rapid  in  the  arms  and  thighs  than  in  the  hands  and  feet. 
The  hemiplegia  is  always  on  the  side  opposite  to  the 
lesion.  This  is  explained  by  the  crossing  of  the  pyra- 
mids in  the  medulla.  A  few  exceptions  to  this  rule  are 
met  with,  and  often  the  parts  on  the  same  side  of  the 
lesion  are  slightly  weakened,  due  to  an  incomplete  cross- 
ing of  the  pyramids  and  the  persistence  of  a  larger 
bundle  in  the  direct  pyramidal  tracts. 

Double  hemiplegia  or  diplegia  is  a  paralysis  of  all  four 
extremities,  and  may  result  from  two  extensive  lesions 
or  a  single  diffuse  lesion  covering  both  hemispheres,  as 
from  meningeal  hemorrhage  in  birth  palsy. 

Common  hemiplegia,  such  as  has  been  described,  is 
not  often  accompanied  with  hemianaesthesia,  but  it  may 
be  associated  with  partial  loss  of  tactile  sensibility  in  the 
extremities  for  a  time,  if  the  lesion  involve  the  sensory 
tracts  lying  far  back  in  the  capsule,  or  when  the  optic 
thalamus  is  injured. 

The  processes  which  most  frequently  give  rise  to 
hemiplegia  are  cerebral  hemorrhage  from  arterial  rup- 
ture, thrombosis,  acute  softening,  embolism,  tumor,  and 
abscess. 

Instead  of  the  face,  arm,  and  leg  being  paralyzed  on 
the  same  side  of  the  body,  it  is  not  very  rare  for  the  face 
to  be  paralyzed  on  one  side  and  the  limbs  on  the  other. 
The  condition  is  known  as  crossed  hemiplegia.  It 
occurs  when  the  lesion  is  so  placed  that  it  interrupts  the 
motor  path  to  the  limbs  above  its  decussation  in  the 
medulla,  and  the  downward  facial  path  of  the  same  side 
after  it  has  crossed  the  median  line  in  the  pons  from  the 
opposite  facial  tract.     The  lesions  must  be  below  the 


92  DISEASES   OF   THE   NERVOUS    SYSTEM. 

middle  of  the  pons,  as  the  crossing  of  the  facial  path 
occurs  just  above.     (See  Fig.  62.) 

This  form  of  paralysis  is  crossed  hemiplegia  in  the 
restricted  sense  of  that  term.  Taken  in  a  wider  sense 
the  term  refers  also  to  the  paralysis  of  one  or  more  of  the 
other  cranial  nerves  onone  side  with  paralysis  of  the  ex- 
tremities of  the  opposite  side.  The  nerves  most  fre- 
quently involved  in  such  a  lesion  are  the  third,  sixth,  and 
seventh.  If  the  third  nerve  is  paralyzed  on  one  side 
and  the  face  and  limbs  on  the  other  the  lesion  is  in  the 
crus  or  presses  on  it  on  the  side  of  the  nerve,  and  this  is 
the  only  situation  in  which  a  lesion  can  cause  such  a 
paralysis.  In  such  cases  the  face  paralysis  has  the 
usual  character  of  a  complete  peripheral  facial  palsy; 
involvement  of  upper  as  well  as  lower  muscles  of  the 
face,  R.  D.,  etc.  (See  Fig.  62  for  explanation  of  these 
anatomic  facts  in  paralysis.) 

Hemiplegia  from  a  disease  in  such  region  is  by  no 
means  always  of  the  crossed  type,  since  there  may  be 
only  a  slight  weakening  of  some  one  or  more  cranial 
nerves,  the  lesion  being  so  small  or  situated  in  the  motor 
tract  only. 

Spinal  Hemiplegia  or  Browh-Sequard' s  Paralysis  is  a 
type  of  hemiplegia  that  results  from  lesions  interrupting 
the  motor  path  of  one  half  of  the  cord.  Both  arm  and 
leg  are  involved  when  the  lesion  is  high  in  the  cord;  the 
paralysis  of  the  leg  may  be  incomplete,  while  that  of  the 
arm  is  complete,  as  fibres  for  the  leg  cross  lower  down 
in  the  cord.  The  lesion  which  causes  spinal  hemiplegia 
is  seldom  confined  to  the  motor  tract  or  even  to  one 
side  of  the  cord.  Hence  there  is  not  only  anaesthesia  on 
the  side  opposite  the  lesion,  but  there  is  commonly  some 
weakening  of  that  side  also.  The  anaesthesia  never  ex- 
tends quite  to  the  level    of    the    lesion,  as  the  sensory 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.         93 

fibres  cross  in  the  cord  a  little  above  their  level  of  en- 
trance. The  symptoms  on  the  side  of  the  lesion  are: 
Motor  palsy,  slight  hypersesthesia  of  skin,  impairment  of 
muscular  sense,  reflex  action  at  first  lessened  and  then 
increased,  and  the  temperature  slightly  raised.  The 
symptoms  on  the  side  opposite  the  lesion  are:  Muscular 
power  nearly  or  quite  normal,  loss  of  skin  sensibility, 
temperature  same  as  that  above  the  lesion.  The  typical 
symptoms  are  less  definite  as  the  lesion  approximates  the 
lumbar  enlargement.  A  lesion  on  one  side  of  the  lumbar 
enlargement  often  affects  sensation  on  the  same  side  as 
motion  because  it  damages  the  sensory  path  before  it  has 
crossed.  In  all  cases  of  crossed  motor  and  sensory 
paralysis  the  sensibility  of  the  muscles  differs  from  the 
other  forms  of  sensibility.  And  if  muscular  sensibility 
is  affected  on  one  side  this  is  the  side  of  the  motor  palsy 
and  not  of  the  cutaneous  anaesthesia. 

Paraplegia  is  a  term  used  generally  to  designate  a 
paralysis  of  both  lower  extremities.  When  all  parts 
below  the  head  are  paralyzed  the  condition  is  termed 
cervical  paraplegia.  The  intercostal  muscles  are  in- 
volved and  respiration  is  diaphragmatic.  Anaesthesia 
may  or  may  not  accompany  paraplegia,  and  there  may 
or  may  not  be  involvement  of  the  bladder  and  rectum. 
The  conditions  which  determine  the  absence  or  presence 
of  these  symptoms  will  be  discussed  elsewhere. 

Paraplegia  is  most  frequently  a  symptom  of  spinal- 
cord  disease,  but  may  result  from  disease  elsewhere.  In 
the  pons  and  medulla  the  motor  tracts  are  close  together, 
and  it  sometimes  happens  that  a  lesion  there  has  suffi- 
cient transverse  extent  to  involve  the  fibres  of  both  sides 
(such  as  tumors),  when  paraplegia  results.  More  rarely 
bilateral  involvement  of  the  crura  leads  to  a  similar  re- 
sult.      Occasionally    paraplegia    results    from    bilateral 


94  DISEASES   OF  THE   NERVOUS   SYSTEM- 

disease  of  the  motor  area  of  the  cortex,  as  that  seen 
in  spastic  paraplegia  of  infants.  It  has  been  already- 
alluded  to  as  double  hemiplegia. 

Paraplegia  is  a  rather  common  occurrence  in  peripheral 
nerve  affections,  as  in  alcoholic  multiple  neuritis.  Com- 
pression of  the  Cauda  equina  by  tumor  or  fracture 
ordinarily  gives  rise  to  it. 

But  paraplegia  is  not  always  referable  to  organic  dis- 
ease. There  is  a  form  known  as  hysterical  paraplegia, 
which  is  a  functional  affection.  A  functional  paraplegia 
from  premature  senile  changes  in  the  arteries  to  the  lower 
part  of  the  cord  and  paraplegia  in  chlorotic  women  some- 
times develops  independently  of  hysteria. 

Monoplegia  signifies  paralysis  of  one  limb  or  of  one 
side  of  the  face,  and,  according  to  the  part  involved,  the 
paralysis  is  termed  a  brachial  monoplegia,  a  crural 
monoplegia,  or  a  facial  monoplegia.  The  lesion  may 
be  cerebral,  spinal,  or  peripheral. 

There  are  certain  general  facts  about  the  distribution 
of  paralysis  which  aid  one  in  determining  whether  a 
palsy  be  of  peripheral,  spinal,  or  cerebral  origin.  If  the 
paralysis  be  confined  to  a  single  muscle  or  group  of 
muscles  known  to  be  innervated  by  a  single  peripheral 
nerve  branch  the  paralysis  is  unquestionably  peripheral. 
If  groups  of  muscles  having  a  certain  function  in  com- 
mon are  involved,  as  for  example  the  dorsal  flexors  or 
adductors  of  the  foot,  the  lesion  is  probably  in  the 
anterior  horn  of  the  spinal  cord,  as  muscle  groups  re- 
lated to  particular  functions  are  represented  in  the  cord. 
When  paralysis  involves  all  the  muscles  of  an  arm  or  leg, 
that  is  of  a  segment  of  the  body,  the  seat  of  the  lesion  is 
probably  the  upper  portion  of  the  motor  path  of  the 
brain,  for  here  movements  of  entire  segments  of  an 
extremity    are    represented    rather    than    of    individual 


SYMPTOMATOLOGY   OF  NERVOUS   DISEASES.        95 

muscles  or  groups  of  muscles.  While  these  general  rules 
are  often  insufficient  in  themselves  to  establish  the  loca- 
tion of  the  lesion  they  should  always  be  taken  into 
consideration. 

It  is  to  be  noted  that  paralysis  when  due  to  lesions  of 
the  central  nervous  system  is  usually  referable  to  disease 
of  a  definite  region.  This  is  especially  true  of  localized 
paralysis,  which  is  consequently  often  spoken  of  as  a 
focal  symptom  in  distinction  to  symptoms  which,  like 
general  convulsions,  point  to  an  extensive  disturbance 
of  function  and  are  hence  called  diffuse.  While  this 
distinction  between  focal  and  diffuse  symptoms  is  useful 
it  cannot  always  be  made  in  practice.  For  example, 
some  symptoms  may  be  signs  of  focal  disease  at  one  time 
and  at  another  of  diffuse  disease.  This  is  the  case  with 
headache  and  with  optic  neuritis. 

The  designation  paralysis  is  correctly  applied  to  all 
grades  of  motor  loss  from  slight  weakness  to  more  or  less 
complete  abolition  of  function.  Sometimes  the  term 
"  paresis  "  is  applied  to  slight  grades  of  weakness.  The 
difference  is  purely  one  of  degree,  and  the  latter  term 
should  not  be  used,  as  it  is  often  employed  in  another 
sense  to  designate  a  form  of  mental  disease.  The  terms 
complete  and  incomplete  are  much  the  better  expressions 
-to  qualify  the  degree  of  paralysis  present  in  any  given 
case  under  description. 

Convulsions. — By  this  term  is  generally  understood 
involuntary,  paroxysmal,  purposeless,  muscular  contrac- 
tion, of  variable  intensity  and  duration  and  of  extensive 
or  limited  distribution. 

Convulsions  may  occur  in  consequence  of  disease  situ- 
ated in  the  cerebrum,  basal  ganglia,  pons,  medulla,  or 
spinal  cord,  but  are  most  often  seen  in  cerebral  dis- 
ease, and  their  relation  to  such  disease  is  of  especial 


9^  DISEASES   OF  THE   NERVOUS   SYSTEM. 

importance.  Convulsions  may  occur  from  disease  of 
any  part  of  the  nervous  system  where  there  is  an  aggre- 
gation of  motor  cells  forming  part  of  a  reflex  arc. 

They  may  arise  (i)  as  a  result  of  active  irritation  of 
brain  tissue,  particularly  of  the  cortex,  such  as  occurs  in 
meningitis  or  meningo-encephalitis  and  active  brain 
tumors;  (2)  in  consequence  of  more  or  less  stationary, 
non-active  lesions,  in  which  some  nerve-cells  are  still 
able  to  generate  nerve  force,  but  do  not  possess  the 
power  of  perfectly  controlling  their  discharge,  as  in 
epileptic  convulsions  following  infantile  cerebral  hemi- 
plegia; (3)  from  spontaneous  discharge  of  nerve  force 
without  a  demonstrable  gross  lesion  or  irritation  in  the 
cortex,  as  in  idiopathic  epilepsy;  (4)  from  discharge  of 
ponto-bulbar  centres  or  from  centres  in  the  cord  itself, 
as  in  myelitis  and  polio-myelitis  resulting  from  an  acute 
morbid  blood  state. 

Convulsions  may  be  local  or  partial  in  their  commence- 
ment, that  is  confined  to  particular  groups  of  muscles  or 
to  one  muscle  of  an  extremity,  and  subsequently  become 
general;  or  they  may  remain  localized  or  be  general  from 
the  beginning. 

General  convulsions  occur  in  organic  disease  of  the 
brain  and  from  a  large  number  of  conditions  external  to 
and  within  the  nervous  system,  which,  when  the  ganglion- 
cells  of  the  cerebral  cortex  are  in  -a  state  of  unstable 
equilibrium  from  defective  nutrition  or  from  other  causes 
such  as  toxic  and  autoxic  agents,  seem  capable  of  deter- 
mining a  discharge  of  nerve  force  from  them,  though 
they  may  be  the  seat  of  no  gross  structural  change. 
Thus  general  convulsions  are  very  commonly  observed 
in  idiopathic  epilepsy,  in  uraemia,  and  especially  in  chil- 
dren at  dentition,  and  at  the  commencement  of  febrile 
diseases,  from  gastro-intestinal  disturbances,  etc.     It  is 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.        97 

an  important  fact  that  a  very  large  majority  of  all  the 
cases  in  which  general  convulsions  occur  are  not  examples 
of  gross  organic  disease  of  the  brain. 

In  organic  disease  of  the  brain  convulsions  are  usually- 
general  when  the  lesion  is  a  diffuse  one  such  as  meningo- 
encephalitis and  not  circumscribed  in  the  motor  area  of 
the  cortex  or  the  subjacent  white  matter.  On  the  other 
hand,  convulsions  that  are  local  in  their  commencement 
or  remain  limited  in  extent  always  indicate  disease  in  or 
adjacent  to  the  motor  area  of  the  cortex.  The  disease 
is  usually  structural  in  character,  but  in  a  few  instances 
no  structural  change  can  be  detected  to  account  for  the 
local  beginning,  and  here  there  are  probably  nutritional 
changes  that  give  rise  to  a  pathological  local  instability. 
In  other  words,  localized  convulsions  constitute  a  focal 
symptom,  general  convulsions  a  diffuse  symptom. 

The  general  convulsions  from  organic  disease  of  the 
brain  bear  a  close  resemblance  to  the  convulsions  of 
idiopathic  epilepsy,  that  is  to  say,  there  is  usually  a. 
period  of  tonic  followed  by  clonic  spasm,  during  which 
the  patient  becomes  rapidly  or  suddenly  unconscious. 
A  focal  beginning  in  a  general  convulsion,  however 
short,  probably  indicates  an  organic  disease  of  the  brain, 
if  uraemia  can  be  excluded. 

In  local  or  partial  convulsions  the  local  onset  is  refer- 
able to  the  nervous  discharge  commencing  at  the  seat  of 
irritation.  Thus  the  spasm  begins  in  one  side  of  the 
face  from  irritation  of  the  facial  centre  and  in  the  arm 
or  leg  from  the  irritation  of  their  respective  centres.  If 
a  convulsion  is  very  slight  it  may  be  limited  to  the 
muscles  in  which  it  begins,  and  there  may  be  no  per- 
ceptible loss  of  consciousness. 

If  of  greater  severity  the  spasm  may  extend  gradually 
or  rapidly  to  other  parts  of  the  side  of  the  body  on  which 

7 


98  DISEASES   OF  THE   NERVOUS   SYSTEM. 

it  begins.  The  order  of  its  extension  is  usually  from  the 
free  end  of  an  extremity  toward  the  trunk,  involving  an 
entire  segment  or  extremity  before  extending  to  other 
parts  of  the  same  side. 

In  such  cases  consciousness  is  usually  lost  as  soon  as 
the  convulsion  is  well  advanced.  The  degree  of  loss  of 
consciousness  and  the  length  of  time  consciousness  re- 
mains absent  is  proportional  to  the  rapidity  and  com- 
pleteness of  nerve  discharge  from  the  cortical  centre.  If 
the  discharge  of  nerve  force  is  of  the  highest  grade  of 

intensity  the  convulsions  may 
involve  both  sides  of  the  body 
at  the  same  time  and  in  such 
cases  loss  of  consciousness  is 
usually  complete  from  the  start. 
Strictly  speaking  it  is  prob- 
able  that    no   convulsions    are 
•    general    from    the    very    com- 
i  mencement.   For  example,  even 
in     infantile     eclampsia      and 
uraemic   convulsions  it  is  very 
common  for  the  spasm  to  begin 

Localized  spasm  of  the  left  side  of   .  •  r  j 

the  face  in  a  patient  suffering  from  lU  OUC  extremity  a  ICW  SCCOndS 
Jacksonian  epilepsy.     (Starr.)  ,       .  .  . 

before  it  passes  to  the  remam- 
ing  half  of  the  body  or  becomes  general.  True  local 
convulsions,  however,  repeatedly  commence  in  one  ex- 
tremity, and  if  they  do  not  remain  local  at  least  con- 
tinue so  for  an  appreciable  time. 

It  is  not  uncommon  for  a  warning  or  aura  to  immedi- 
ately precede  a  convulsive  attack.  The  aura  is  always 
sensory  in  character  and  often  begins  in  the  part  which 
is  afterwards  the  seat  of  convulsion,  and  this  is  particu- 
larly true  if  there  be  a  general  convulsion  with  a  local 
onset.     The   sensation    may   ascend   the   limb  first  in- 


FIG.  02. 


SYMPTOMATOLOGY   OF   NERVOUS    DISEASES.        99 

volved,  and  even  pass  to  the  second  extremity  affected, 
before  the  convulsion  comes  on.  Such  sensory  aurae 
undoubtedly  result  from  a  nervous  discharge  from  sen- 
sory cells  which  precedes  that  which  occurs  from  motor 
nerve-cells,  the  functional  control  of  which  is  one  of 
their  chief  functions.  The  motor  area  of  the  cortex 
contains  sensory  as  well  as  motor  cells,  and  the  presence 
of  a  sensory  aura  before  the  spasm  indicates  that  the 
convulsion  has  its  initiative  in  sensory  elements,  that 
is;  cerebral  convulsions  are  a  sensory-motor  reflex  and 
are  largely  sensory  in  origin  with  a  resultant  motor 
expression. 

Aurae  of  the  special  senses,  as  a  flash  of  light,  an  odor, 
or  a  sound,  are  not  uncommon  in  idiopathic  epilepsy, 
but  they  are  of  relatively  rare  occurrence  in  organic  dis- 
ease of  the  brain.  When  they  do  occur  they  indicate 
that  the  lesion  has  its  maximum  intensity  at  or  near  the 
special  sense  centre  corresponding  to  the  aura — in  the 
occipital  lobe  when  there  is  a  visual  aura,  etc. 

Slight  weakness  in  the  part  or  parts  involved  is  usual 
after  a  local  or  partial  convulsion.  If  the  convulsions 
recur  frequently  at  short  intervals  the  weakness  may  be 
very  decided.  In  most  cases  it  soon  passes  away,  but 
in  rare  instances  permanent  paralysis  may  result.  In 
such  cases  the  convulsions  have  probably  given  rise  to 
a  destructive  lesion  by  hemorrhage.  If  the  convulsions 
happen  to  involve  the  extremities  of  one  side  of  the  body 
the  weakness  is,  as  might  be  expected,  hemiplegic,  but 
it  is  readily  distinguished  from  hemiplegia  by  wearing 
off  in  two  or  three  days  or  earlier.  The  weakness  fol- 
lowing convulsions  is  called  post-convulsive  or  exhaus- 
tion paralysis.  It  is  explained  on  the  supposition  that  a 
severe  convulsive  seizure  exhausts  the  motor  nerve-cells 
related  to  the  part.     The  resultant  paralysis  is  greatest 


lOO         DISEASES    OF   THE   NERVOUS   SYSTEM. 

in  those  particular  parts  which  are  most  actively  engaged 
in  the  preceding  convulsions.  Exhaustion  paralysis 
occurs  most  frequently  in  those  cases  suffering  from  a 
previous  incomplete  organic  hemiplegia  of  children  in 
which  epileptic  convulsions  have  been  superinduced  in 
later  life.  The  general  exhaustion  seen  after  general 
convulsions  is  probably  analogous  in  cause  and  effect  to 
the  weakness  which  occurs  in  certain  parts  following 
local  convulsion. 

As  to  the  diagnostic  significance  of  local  convulsions 
it  may  be  said  that  this  is  the  same  whether  the  convul- 
sions remain  localized  or  subsequently  become  unilateral 
or  general.  They  do  not  quite  prove  the  presence  of 
structural  disease  because  in  rare  instances  idiopathic 
epilepsy,  ursemic  convulsions,  and  diabetic  convulsions 
may  begin  locally.  But  every  case  where  convulsions 
begin  locally  should  excite  suspicion  of  organic  disease 
and  should  lead  to  a  minute  and  careful  search  for  it.  It 
is  also  to  be  noted  that  the  significance  of  repeated  local 
convulsion  is  not  diminished  by  the  occurrence  of  general 
convulsions  at  other  times. 

Convulsions  which  are  general  from  the  commence- 
ment, on  the  contrary,  point  to  idiopathic  epilepsy.  But 
they  do  not  exclude  the  possibility  of  structural  disease, 
because  general  convulsions  are  not  uncommonly  symp- 
toms of  organic  diseases  of  the  brain.  In  such  cases  the 
distinction  must  be  made  by  establishing  the  presence 
or  absence  of  other  symptoms  of  organic  disease.  It 
cannot  be  made  from  the  character  of  convulsions  alone. 

General  convulsions,  besides  being  met  with  in  organic 
diseases  of  the  brain  and  spinal  cord,  are  observed  in 
idiopathic  epilepsy,  tetanus,  uraemia,  diabetes,  and 
hysteria.  It  is  not  very  uncommon  for  hysterical  con- 
vulsions to  occur  in  the  course  of  organic  disease  of  the 


SYMPTOMATOLOGY    OF   NERVOUS    DISEASES.       lOI 

brain,  and  this  sometimes  leads  to  errors  in  diagnosis. 
Such  convulsions  not  rarely  result  in  the  course  of  intra- 
cranial tumors;  occasionally  they  are  seen  in  meningitis. 

Localized  convulsions  (monospasm,  hemispasm)  are 
much  more  frequently  met  with  in  intracranial  tumor 
than  in  any  other  form  of  disease.  The  neoplasm 
causing  them  is  usually  situated  very  near  the  motor 
cortex  and  usually  quite  superficially.  When  the  tumor 
is  situated  at  a  considerable  distance  from  the  motor 
area  the  local  convulsions  are  probably  the  result  of 
meningitis  over  the  cortex. 

Convulsions  are  frequently  classified  on  a  purely 
mechanical  basis  according  as  the  tonic  or  clonic  ele- 
ment predominates.  Clonic  spasm  does  not  necessarily 
differ  from  tonic  convulsion  in  its  origin  or  essential 
character,  but  the  impulses  in  the  nerve  discharge  are 
infrequent  enough  to  permit  the  muscular  apparatus  a 
temporary  intermittent  relaxation.  A  tonic  or  tetanic 
convulsion  is  one  in  which  the  muscular  contraction 
continues  for  an  appreciable  but  short  period  of  time. 
Such  spasm  is  met  with  in  many  conditions,  for  example 
at  the  onset  of  a  grand  mal  epileptic  paroxysm,  in  some 
cases  of  petit  mal,  in  major  hysteria,  and  in  tetanus. 
Tetanic  seizures  lasting  for  hours  or  even  days  some- 
times result  from  disease  involving  the  gray  matter  in 
the  floor  of  the  fourth  ventricle  and  perhaps  from  cere- 
bellar disease  and  secondary  pressure  on  the  cruri. 
From  their  resemblance  to  tetanus  the  convulsions  are 
often  designated  tetanoid. 

Purely  tonic  spasm  (Trousseau's  symptom)  may  be 
excited  by  pressure  on  the  larger  nerves  and  arteries,  as 
in  laryngismus  stridulus.  The  mechanical  and  elec- 
trical irritability  of  the  peripheral  nerves  is  increased 
during  the  intervals. 


I02         DISEASES    OF   THE   NERVOUS    SYSTEM. 

Localized  tonic  spasm  is  sometimes  a  symptom  of  con- 
siderable importance.  It  is  seen  as  trismus  (spasm  of  the 
muscles  of  mastication),  in  tetanus  (early  symptom),  in 
some  cases  of  hysteria,  and  sometimes  in  meningitis. 
Tonic  spasm  of  the  calf  muscles  (cramp)  is  observed  in 
hysterical,  neurasthenic,  and  alcoholic  subjects  as  a  con- 
sequence of  over-use  of  these  muscles.  Another  form  of 
tonic  spasm  is  that  of  the  sterno-cleido-mastoid,  causing 
"wry-neck." 

When  tonic  spasm  is  of  considerable  duration  or  of 
gradual  onset,  it  is  perhaps  more  properly  spoken  of  as 
rigidity,  and  will  be  considered  under  this  tjtle  (p.  92), 
although  it  must  be  understood  that  a  sharp  distinction 
cannot  always  be  made. 

Clonic  convulsions  are  characterized  by  the  rapidly  in- 
termittent character  of  the  muscular  contractions  which 
produce  them.  They  are  distinguished  from  tremor  by 
being  usually  wider  in  range,  less  rhythmical  in  character, 
and  of  shorter  duration  ;  but  here  again  the  distinction 
between  the  two  kinds  of  spasm  is  not  always  absolute. 

Clonic  convulsions  occur  in  various  forms  in  a  great 
variety  of  morbid  conditions  of  the  nervous  system,  alone, 
or  with  those  that  are  tonic.  In  the  condition  known  as 
paramyoclonus  multiplex  we  sometimes  have  examples  of 
purely  clonic  convulsions.  In  this  disease  there  is  rapidly 
repeated  clonic  spasm  occurring  at  varying  intervals. 
The  spasms  vary  from  50  to  180  per  minute,  and  involve 
several  muscles  of  a  physiological  group  at  once,  thus 
giving  the  appearance  of  purposive  action. 

The  term  "  internal  convulsions  "  has  been  applied,  not 
inaptly,  to  conditions  of  muscular  spasm  in  internal  organs. 
Thus,  the  laryngeal  spasm  of  rickety  children,  known  as 
laryngismus  stridulus,  may  be  regarded  as  analogous  to 
the  general  convulsions  which  sometimes  occur  in  these 


SYMPTOMATOLOGY    OF   NERVOUS   DISEASES.      I03 

same  subjects.     The  spasm  is  thought  to   result  from 
discharges  from  lower  nervous  centres  in  the  medulla. 

Tremor. — Tremor  or  trembling  may  be  defined  as  a 
rapid  involuntary  to-and-fro  movement  of  a  part  resulting 
from  the  alternate  and  usually  rhythmical  contraction  of 
antagonistic  muscles.  Tremor  in  the  strict  sense  of  the 
word  is  always  an  oscillation  of  narrow  range.  It  may  or 
may  not  be  present  when  the  part  in  which  it  occurs  is 
at  rest — most  tremors  are  not  then  present.  The  tremor 
of  paralysis  agitans  usually  continues  during  rest,  and 
the  tremor  which  results  from  cold  and  from  emotion 
originates  when  the  body  is  at  rest.  The  majority  of 
tremors  continue  during  voluntary  motion  and  are  in- 
creased by  the  extra  muscular  tension.  The  tremor  of 
paralysis  agitans  may  be  inhibited  at  will  by  voluntary 
effort  for  a  short  time,  but  it  soon  recommences. 

The  term  **  intention  tremor,"  borrowed  from  the 
Germans,  is  used  to  designate  tremors  which  occur  only 
during  voluntary  movement  causing  increased  muscle 
tension.  It  is  more  accurately  named  action  tremor. 
It  is  frequently  seen  in  disseminated  sclerosis  and  in 
mercurial  poisoning.  It  is  often  wide  in  range,  irregular 
in  rhythm,  and  ataxic  in  character. 

Roughly  speaking,  the  extent  of  a  tremor  is  inversely 
proportionate  to  its  rapidity,  but  the  same  tremor  may 
vary  somewhat  in  range  at  different  times.  There  is 
considerable  difference  in  the  rapidity  of  different  kinds 
of  tremor,  and  these  differences  are  sufficiently  constant 
to  be  of  some  diagnostic  value.  For  instance,  the  tremor 
of  alcoholism  is  rapid  and  varies  from  seven  to  eight, 
and  that  of  paralysis  agitans  from  four  to  seven  per 
second.  Tremor  is  a  symptom  in  a  variety  of  diseases 
of  the  nervous  system.  It  is  sometimes  the  result  of 
organic  disease,  but  is  commonly  met  with  in  diseases  of 


I04         DISEASES   OF   THE   NERVOUS   SYSTEM. 

a  nutritional  character  in  which  no  gross  structural 
changes  in  the  nervous  elements  have  been  detected. 
Thus  it  is  seen  on  the  one  hand  in  disseminated  sclerosis 
after  hemiplegia,  in  senile  dementia,  and  certain  forms 
of  toxic  neuritis;  and,  on  the  other  hand,  after  exhaust- 
ing diseases,  in  neurasthenia,  paralysis  agitans,  hysteria, 
and  Basedow's  disease.  Very  frequently  tremor  is  a 
toxic  symptom,  and  as  such  it  is  seen  in  alcoholism,  in 
poisoning  from  lead,  mercury,  opium,  cocaine,  and  after 
the  excessive  use  of  tea,  coffee,  tobacco,  and  quinine. 

But  tremor  is  also  encountered  in  cases  where  no  as- 
signable exciting  cause  can  be  detected  and  in  which 
there  is  no  associated  abnormal  state.  It  is  sometimes 
not  only  congenital  but  also  hereditary,  and  may  be 
present  throughout  a  lifetime  without  any  other  nervous 
affection  being  present.  It  may  affect  several  members 
in  a  family  through  several  generations.  Sometimes  this 
simple  tremor,  as  it  is  called,  seems  to  be  related  to 
emotion  or  to  prolonged  anxiety,  and  not  infrequently  a 
neuropathic  heredity  can  be  traced.  Simple  tremor 
neither  shortens  life  nor  influences  the  general  health. 
Senile  tremor  occurs  in  extreme  old  age  or  in  early 
senility,  and  while  it  does  not  exhibit  the  same  rigidity 
and  muscular  weakness  observed  in  paralysis  agitans  it 
is  doubtless  closely  associated  and  probably  dependent 
upon  an  allied  structural  change  in  the  nerve  elements. 
Most  tremors  cease  during  sleep;  rarely  a  tremor  is  di- 
minished or  unaffected.  The  upper  extremities  are 
most  frequently  the  seat  of  tremor,  and  the  head  is  more 
involved  than  the  leg. 

With  regard  to  the  pathology  of  tremor  nothing  defi- 
nite can  be  said.  We  know  that  when  a  voluntary 
movement  is  made  every  contraction  of  one  set  of 
muscles  is  accompanied  by  a  corresponding  relaxation  of 


SYMPTOMATOLOGY    OF   NERVOUS   DISEASES.      IO5 

antagonistic  muscles.  This  arrangement  serves  to  make 
motion  even  and  regular  and  is  doubtless  subserved 
by  a  close  anatomical  association  in  corresponding 
motor  centres.  A  continuous  voluntary  muscle  con- 
traction probably  consists  of  a  series  of  single  contractions 
following  each  other  at  very  short  intervals,  due  to  inner- 
vating impulses  from  the  cerebral  cortex,  which  are 
liberated  at  the  rate  of  about  ten  or  twelve  per  second, 
according  to  the  position  in  which  they  are  generated. 
So  long  as  these  impulses  follow  one  another  rhythmi- 
cally, and  simultaneously  reach  the  antagonistic  muscles 
involved  in  a  voluntary  movement,  the  motion  is  a  con- 
tinuous one.  It  is  conceivable  that  the  nice  mechanism 
in  which  these  simultaneous  liberations  of  nerve  force 
occur  may  be  readily  deranged  to  a  slight  degree  by 
nutritional  disease  which  is  far  short  of  being  a  gross 
structural  change  and  that  the  parallelism  of  the  inner- 
vating rhythm  in  opposed  muscles  would  suffer  slight 
derangement.  The  opposing  muscles  would  then  act, 
not  simultaneously,  but  alternately,  and  the  expres- 
sion of  such  alternation  would  be  tremor.  But  the 
disturbance  of  the  cortical  gray  matter  in  the  brain  in 
which  motor  impulses  are  controlled  and  generated  is 
probably  not  the  only  manner  in  which  tremor  may 
arise.  Structural  changes  in  the  nerves  which  con- 
duct voluntary  impulses  may  damage  the  axis-cylinders 
enough  to  modify  without  destroying  their  conductivity 
and  it  is  probable  that  some  forms  of  tremor,  as  that  of 
disseminated  sclerosis  and  of  neuritis,  depend  on  such 
interference  with  conduction.  The  majority  of  tremors, 
however,  undoubtedly  depend  on  nutritional  alterations 
and  less  commonly  on  structural  changes  in  sensory  in- 
hibiting cells  in  the  cerebral  cortex.  There  is  good  rea- 
son to  believe — although  the  evidence  is  not  conclusive 


I06         DISEASES   OF   THE   NERVOUS   SYSTEM. 

—  that  in  paralysis  agitans,  dementia  paralytica,  hys- 
teria, fear,  and  in  alcoholism  the  tremor  is  of  cortical 
origin.  Inasmuch  as  the  pathology  of  tremor  is  still 
obscure  its  diagnostic  significance  is  somewhat  vague. 
Roughly  speaking  tremor  is  to  be  regarded  as  one  evi- 
dence of  nutritional  derangement  of  functions  of  the 
sensory-motor  cortex,  which  may  or  may  not  present 
gross  structural  changes.  More  cannot  be  said.  In 
order  to  determine  the  location  of  the  lesion  and  whether 
the  change  is  simply  one  of  nutrition  and  not  one  of  gross 
structural  change,  the  conditions  associated  with  the 
tremor  must  be  interrogated.  Not  infrequently  these 
points  cannot  be  decided.  Myographic  tracings  of  vari- 
ous forms  of  tremors  are  shown  in  Fig.  63. 

Fibrillation. — Fibrillary  twitchings  or  fibrillations 
are  involuntary  contractions  of  small  numbers  of  muscle- 
fibres.  As  they  give  rise  to  no  movements  of  the  parts 
in  which  they  occur,  they  are  recognized  only  when 
occurring  in  muscle-fibres  which  lie  just  beneath  the 
skin.  The  contraction  appears  as  a  small  wave-like 
elevation  running  rapidly  along  the  muscle  in  which  it 
occurs.  It  may  be  confined  to  a  part  of  one  muscle  or 
may  be  seen  in  all  the  muscles  of  an  extremity.  It  is 
chiefly  met  with  in  the  extremities,  face,  and  tongue. 
The  contractions  may  be  almost  constant  or  may  be 
separated  by  considerable  intervals.  It  is  often  easy  to 
produce  them  at  will  by  cooling  or  tapping  the  skin  over 
the  muscles.  In  those  conditions  giving  rise  to  fibrilla- 
tion the  mechanical  irritability  of  the  muscle-fibres  is 
increased.  Fibrillary  tremors  occur  under  two  dis- 
tinctly different  clinical  conditions — as  the  expression  of 
general,  slight,  functional  derangement  of  the  nervous 
system  and  as  the  result  of  a  degenerative  process  in  the 
muscle-fibres.       Thus   it    is    met    with   in   neurasthenic 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.       lO/ 


FIG.   63. 

Myographic  tracing  of  various  forms  of  tremor  taken  directly  from  the  moving 
parts.  Reduced  to  one  half,  i,  tremor  after  hemiplegia,  very  fine,  rather  irreg- 
ular ;  2-6,  paralysis  agitans — 2  and  3,  very  fine  tremor,  4,  5,  6,  coarse  tremor ; 
7,  insular  sclerosis,  very  irregular  in  range,  although  in  time  ;  8,  general  paralysis 
of  the  insane  ;  9,  hysterical  tremor.    (Gowers. ) 


lo8         DISEASES   OF  THE   NERVOUS   SYSTEM. 

persons  who  are  free  from  organic  disease  and  after 
excessive  exercise  or  excessive  venery.  Under  these 
circumstances  the  contractions  are  usually  infrequent 
and  not  confined  to  any  particular  group  of  muscles; 
but  they  are  sometimes  very  persistent- and  frequent, 
with  a  tendency  to  involve  particular  muscle  groups. 
On  the  other  hand,  almost  any  lesion  which  gives  rise  to 
degenerative  muscular  atrophy  is  capable  of  causing  fibril- 
lary twitchings  in  the  atrophied  muscles.  For  example, 
primary  muscular  atrophy  and  degenerative  neuritis  are 
common  causes  of  fibrillation.  It  ceases  in  polio-myelitis 
when  the  atrophic  muscle-fibres  are  extensively  atro- 
phied; it  therefore  does  not  last  long  in  acute  lesions. 
In  progressive  muscular  atrophy  it  is  especially  frequent 
and  persists  through  a  long  period  of  time  as  the  process 
of  atrophy  is  a  slow  one.  The  fibrillation  is  usually  fre- 
quent and  persistent  and  is  always  localized  in  the  wasted 
muscle. 

Fibrillary  twitchings  are  of  course  not  pathognomic  of 
chronic  muscular  atrophy,  as  has  been  held,  nor  are  they 
an  absolutely  constant  accompaniment  of  this  disease. 
Fibrillation  may  occur  in  atrophic  diseases  before  the 
muscles  give  any  appreciable  evidence  of  wasting. 

Certain  drugs,  as  aconitia,  physostigmine,  and  pilo- 
carpine, may  cause  fibrillary  twitchings,  probably  by 
irritating  the  motor-end  plates  in  the  muscles. 

Fibrillation  is  generally  due  to  irritation  or  destruction 
of  nerve-endings  or  of  the  trophic  centres  of  the  cord  in 
the  anterior-horn  cells.  Fibrillary  twitchings  seldom  or 
never  occur  in  the  pure  types  in  muscular  distrophies. 

Rigidity. — The  tonic  muscular  spasm,  which  shows 
itself  as  rigidity  in  one  or  more  extremities  or  in  the 
muscles  of  the  trunk,  is  met  with  in  both  nutritional  and 
structural  diseases  of  the  nervous  system.     It  occurs  in 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      IO9 

the  tonic  convulsive  seizures  of  epilepsy  and  hysteria, 
and  is  seen  widely  distributed  in  tetanus.  These  par- 
ticular forms  have  been  considered  under  convulsions. 
Here  will  be  considered  especially  the  rigidity  of  organic 
disease  of  the  nervous  system  and  the  somewhat  rare 
condition  of  catalepsy. 

Rigidity  occurs  as  a  symptom  of  so  many  widely  differ- 
ent diseases  of  the  nervous  system  that  some  explanation 
of  the  general  pathological  processes  which  may  give  rise 
to  it  will  facilitate  an  understanding  of  its  occurrence. 

Rigidity  may  result  from  an  active  irritative  process 
anywhere  in  the  motor  path — in  its  upper  or  its  lower 
segment.  The  increased  muscle  tone  giving  rise  to 
rigidity  is  called  hypertonicity.  The  rigidity  of  menin- 
gitis is  an  example  of  its  occurrence  from  irritation  of 
the  upper  part  of  the  motor  path  in  the  cortex.  Menin- 
geal irritation  is,  however,  capable  of  diminishing  the 
tonus  of  muscles  (hypotonus)  instead  of  increasing  it. 
Rigidity  is  then,  of  course,  absent;  the  muscles  may, 
indeed,  be  quite  flaccid. 

The  rigidity  which  occurs  subsequent  to  lesions  of 
the  internal  capsule  (commonly  hemorrhage  or  secondary 
softening)  is  also  the  result  of  the  irritation  which  attends 
them  and  involves  the  extremities  which  are  the  seat  of 
the  hemiplegia.  This  is  true  also  of  disease  in  any  part 
of  the  pyramidal  tract  below  the  capsule.  When  rigidity 
comes  on  immediately  after  the  onset  of  the  hemiplegia 
and  lasts  only  a  few  or  several  hours  it  is  called  initial 
rigidity;  when  it  appears  within  a  few  days  of  the  onset 
and  lasts  two  or  three  weeks  it  is  spoken  of  as  early 
rigidity.  Usually  the  early  rigidity  is  slight  in  degree, 
occasionally  it  is  very  marked.  Neither  early  nor  initial 
rigidity  is  a  constant  accompaniment  of  hemiplegia.  Both 
forms  are  certainly  the  result  of  irritation — initial  rigidity 


no         DISEASES    OF   THE   NERVOUS   SYSTEM. 

resulting  from  the  mechanical  irritation  and  shock  of 
motor  fibres  by  the  lesion  that  interrupts  their  conti- 
nuity, early  rigidity  from  the  inflammation  which  often 
follows.  Lesions  which  may  produce  irritation  and 
therefore  rigidity  in  the  pyramidal  tracts  of  the  cord 
are  rather  uncommon.  External  cord  lesions  however 
are  common  (meningitis,  compression  paraplegia  from 
tumors)  and  rigidity  is  a  frequent  accompaniment  of 
such  affections. 

But  there  is  an  influence  other  than  irritation  which 
is  a  common  cause  of  rigidity.  The  normal  lone  of 
muscles  depends  on  the  integrity  of  the  ganglion-cells 
of  the  anterior  horns  with  which  they  are  connected. 
Destruction  of  these  cells  results  not  only  in  paralysis  of 
the  muscles  but  in  a  loss  of  tone,  as  evidenced  by  their 
relaxation.  Now  these  ganglion-cells  are  capable  under 
normal  circumstances  of  liberating  more  nervous  energy 
than  is  required  to  give  the  muscles  their  normal  tonicity, 
and  are  continually  held  in  check  or  inhibited  to  prevent 
such  overaction,  by  stimuli  descending  the  pyramidal 
tracts  from  the  cortex  of  the  brain.  If  these  inhibitory 
stimuli  are  cut  off  by  the  processes  of  disease,  overaction 
of  the  spinal  centres  is  the  necessary  result.  There  is 
hypertonicity  or  rigidity  of  the  muscles.  This  rigidity" 
may  be  constant,  or  it  may  diminish  considerably  during 
rest.  Degeneration  of  the  pyramidal  tracts  effectu- 
ally interrupts  the  inhibition  from  the  higher  centres, 
and  hence  it  is  that  we  find  rigidity  in  the  many  types  of 
disease  in  which  such  degeneration  occurs.  After  hemi- 
plegia, for  example,  there  occurs  a  secondary  degenera- 
tion of  the  pyramidal  tract  in  which  the  lesion  lies.  In 
the  course  of  a  few  weeks  the  rigidity  appears, — late 
rigidity  it  is  termed, — and  remains  for  months  or  years. 
If  the  degeneration  be  great  in  degree  the  rigidity  may  be 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      Ill 

permanent.  A  similar  secondary  degeneration  may  re- 
sult from  interruption  of  the  fibres  in  the  pons,  medulla, 
or  cord,  from  hemorrhage,  softening,  or  inflammation. 
The  primary  degeneration  of  the  pyramidal  tracts  in  the 
cord  as  seen  in  lateral  sclerosis  also  gives  rise  to  rigidity 
in  paralyzed  muscles.  In  the  case  of  amyotrophic  lateral 
sclerosis  the  presence  of  rigidity  depends  on  the  condi- 
tion of  the  ganglion-cells  of  the  anterior  cornua.  If 
these  are  only  slightly  injured  and  can  still  maintain  the 
muscle  tonus,  this  is  increased  by  the  degeneration  in 
the  lateral  tract.  If  they  are  so  extensively  altered  as 
to  lose  their  control  of  the  muscle  tonus,  no  degree  of  de- 
generative change  in  the  lateral  tracts  is  capable  of  re- 
storing or  increasing  the  muscular  tone.  Hence  it  is 
that  we  have  a  tonic  type  of  chronic  muscular  atrophy. 
(See  p.  450.) 

In  general,  we  may  say  that  rigidity  is  due  to  irritation 
of  motor  structures  in  acute  processes,  and  to  deficient 
control  of  the  reflex  mechanism  which  subserves  muscu- 
lar tone,  in  chronic  forms  of  disease. 

The  motor  overaction  is  seldom  equal  in  degree  in 
antagonistic  muscle  groups.  Either  the  flexors  or  the 
extensors  predominate  and  determine  the  position  of 
the  limb.  If  the  spasm  causes  persistent  shortening  of 
a  certain  set  of  muscles  the  resulting  condition  is  a 
contracture. 

Contracture  and  Contraction. — These  words  are 
used  in  different  senses  by  different  authors,  and  this  has 
given  rise  to  considerable  confusion.  According  to  the 
best  English  usage  the  word  co7itracture  is  applied  to  the 
shortening  of  a  muscle  or  group  of  muscles  from  active 
contraction  of  the  muscular  fibres,  and  not  from  struc- 
tural changes  in  these  fibres.  The  contracture  may  last 
for  a  few  minutes  or  for  years.      Good   examples  of 


112         DISEASES   OF   THE   NERVOUS   SYSTEM. 

contracture  are  seen  in  cerebral  tumor  involving  the  motor 
tract,  in  the  late  rigidity  of  hemiplegia,  and  in  hysteria. 
The  contracture  of  hysteria  may  persist  many  years.  A 
contracture  can  always  be  overcome  temporarily  by 
gentle,  firm  extension  of  the  muscle. 

A  contraction  is  the  shortening  of  a  muscle  or  group 
of  muscles  from  structural  changes  in  the  muscle-fibres 
— structural  contracture  it  is  sometimes  called,  A  con- 
traction cannot  be  reduced  by  extension.  Contraction 
of  a  muscle  from  structural  changes  is  always  preceded 
by  a  period  o.  active  contracture  in  which  connective- 
tissue  alterations  have  not  yet  occurred.  The  causes  of 
contraction  are: 

a.  The  unequal  paralysis  of  antagonistic  muscles. 
The  stronger  muscles  assert  themselves  and  give  rise  to 
serious  deformity  of  the  limb,  though  there  is  no  spasm. 
This  is  often  seen  in  poliomyelitis. 

b.  From  long-continued  spasmodic  contracture  from 
any  cause  whatever.  The  structural  changes  in  such 
cases  develop  very  slowly — often  not  until  many  years 
have  passed.  Such  structural  changes  occur  even  from 
hysterical  contracture  in  some  of  the  rare  instances  in 
which  such  contracture  has  existed  unaltered  for  years. 

Since  contractures  are  generally  associated  with  some 
degree  of  motor  weakness,  even  when  they  result  from 
spasm,  they  are  often  regarded  as  late  conditions  of 
paralysis,  though  it  is  to  be  remembered  that  they  some- 
times occur  independently  of  motor  loss.  Contractures 
may  result  from  paralysis  of  cerebral,  spinal,  or  periph- 
eral origin.  By  far  the  most  common  cerebral  cause 
of  contracture  is  hemiplegia.  The  contracture  is  pro- 
duced by  the  late  rigidity  already  mentioned.  In  the 
upper  extremity  the  position  which  results  from  the  con- 
tracture is  one  in  which  there  is  flexion  of  the  elbow  and 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      II3 

pronation  of  the  wrist,  and  flexion,  often  great,  of  the 
fingers,  especially  of  the  second  and  third  phalanges. 
By  passively  flexing  the  wrist  these  phalanges  can  be 
readily  extended  because  such  flexion  lengthens  the 
course  of  the  flexor  tendons,  but  if  the  wrist  is  extended 
somewhat,  the  fingers  return  to  their  original  state  of 
flexion.  The  contracture  thus  preponderates  in  the 
flexors,  but  there  is  usually  some  rigidity  in  the  extensors. 
In  the  leg  there  is  usually  extensor  contracture,  the  an- 
tagonistic muscles  being  much  more  equally  balanced, 
and  the  leg  is  straight.  In  the  foot  there  is  a  tendency, 
often  marked,  to  take  the  position  of  talipes  equinus  or 
equino-varus. 

The  great  cause  of  contracture  from  spinal-cord  dis- 
ease is  poliomyelitis,  and  especially  the  infantile  form. 
It  is  unusual  for  all  the  muscles  of  an  extremity  to  be 
involved  or  to  be  involved  equally.  In  the  lower  ex- 
tremity the  tibialis  anticus  and  peronei  suffer  most  fre- 
quently and  there  is  a  resulting  contracture  of  the  calf 
muscles,  which  are  either  unparalyzed  or  only  slightly 
involved.  Hence  talipes  equinus  results;  and  it  is 
equino-varus  or  equino-valgus  according  as  the  peroneal 
group  or  the  tibialis  anticus  is  most  involved.  When 
the  calf  muscles  suffer  most,  as  they  occasionally  do, 
talipes  calcaneus  results.  In  the  arm  contractures  are 
much  less  apt  to  result  than  in  the  leg,  and  when  they 
do  occur  give  rise  to  less  deformity. 

The  contracture  of  poliomyelitis  early  becomes  struc- 
tural contracture. 

Contracture  from  disease  of  the  peripheral  nerves  is 
not  common.  It  occurs  chiefly  as  the  result  of  long- 
continued  irritation,  especially  of  the  anterior  nerve- 
roots,  or  as  the  result  of  injury  to  motor  nerves. 

Catalepsy. — This  is  a  condition  of  infrequent  occur- 


114 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


rence  in  organic  disease  of  the  nervous  system.  It  is 
practically  confined  to  major  hysteria  and  to  the  kata- 
tonic  stupor  of  dementia  precox.  Trance,  lethargy, 
tetanic  rigidity,  and  cerea  flexibilitas  are  all  states  of 
the  same  general  condition.  Catalepsy  may  be  defined 
as  a  state  of  general  or  local  muscular  rigidity  as- 
sociated with  a  state  of  perverted  consciousness.  It 
may  occur   spontaneously  in  disease   or  it  may   be  in- 


FIG.   64. 
A  case  of  catalepsy  (Dana), 


duced  in  a  state  of  hypnotism.  It  has  been  noted  in 
brain  abscess,  tumor,  hemorrhage,  softening,  and  men- 
ingitis, but  only  when  consciousness  has  been  much  im- 
paired. Its  practical  diagnostic  significance  at  present 
is  confined  to  hysteria  and  the  adolescent  insanities.  In 
the  absence  of  hysterical  stigma  and  the  presence  or  a 
history  of  stupor,  negativism,  automatism,  excitement 
alternating  with  depression,  stereotypy,  verbigeration, 
etc.,  it  points  to  pronounced  mental  disease.    In  the  latter 


SYMPTOMATOLOGY    OF   NERVOUS   DISEASES.      II5 

disease  the  origin  of  the  katatonic  stupor  is  commonly 
rapid  with  partial  or  complete  obscuration  of  conscious- 
ness. The  features  grow  expressionless,  the  respiratory- 
movements  and  heart  action  are  depressed.  The  volun- 
tary impulses  seem  to  be  overcome  by  counter  impulses. 
An  act  may  be  begun  but  almost  immediately  is  checked 
by  a  counter  impulse  which  produces  an  act  contrary  to 
the  one  desired. 

Athetosis  and  Athetoid  Movements. — The  word 
athetosis  (meaning,-  "without  form")  was  introduced  to 
designate  a  peculiar  form  of  chronic  spasm — "mobile 
spasm"  it  has  been  aptly  called — which  gives  rise  to 
slow,  irregular  inco-ordinated  movements.  The  move- 
ments usually  involve  the  hand  and  foot,  sometimes 
also  the  face,  but  they  are  always  most  marked  in  the 
hand.  In  distribution  the  movements  may  be  either 
strictly  confined  to  one  side  of  the  body,  or  rarely  they 
may  be  bilateral. 

This  condition  of  athetosis  has  been  looked  upon  as  a 
primary  type  of  disease  since  it  is  said  to  occur  occa- 
sionally in  persons  apparently  healthy,  unassociated  with 
any  other  abnormal  state. 

Movements  of  essentially  the  same  character  as  those 
of  athetosis  are  not  infrequently  seen  as  a  post-hemiplegic 
condition.  They  are  often  met  with  in  children  and 
sometimes  in  adults.  As  in  athetosis  they  affect  the 
hand  more  often  and  in  greater  degree  than  the  foot. 
Usually  the  lesion  which  causes  them  is  unilateral  and 
hence  the  movements  are  generally  one-sided.  When 
the  lesion  is  bilateral  the  movements  may  involve  both 
sides  of  the  body.  These  "athetoid  movements,"  as 
they  are  called,  never  occur  while  the  hemiplegia  re- 
mains absolute,  but  develop  with  the  return  of  volun- 
tary power,  usually  some  months  after  the  onset  of  the 


Examples  of  the  position  of  the  fingers  in  the  movements  of  athetosis  (personal 
observation).     (Strumpell.) 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      II7 

paralysis.  There  is  commonly  associated  with  these  spas- 
modic movements  a  certain  amount  of  muscular  rigidity 
which  tends  to  give  to  the  part  some  particular  attitude, 
and  this  rigidity  is  related  to  the  degree  of  paralysis — 
being  slight  when  the  weakness  is  inconsiderable.  The 
recognition  of  the  dependence  of  this  symptomatic  form 
of  athetosis,  as  it  may  be  termed,  upon  a  cerebral  lesion 
is  usually  not  difficult.  The  history  of  a  hemiplegic  at- 
tack, the  loss  of  power  and  rigidity  in  the  extremity 
which  is  the  seat  of  the  athetoid  movements,  and  in 
children  the  arrest  of  development  in  bone  and  muscle, 
all  point  clearly  to  an  organic  cerebral  process.  But  it 
is  well  known  that  a  slight  lesion,  especially  during 
childhood,  may  be  so  .far  recovered  from,  in  the  course 
of  time,  that  there  remain  only  slight  objective  evidences 
of  a  cerebral  process.  Under  these  circumstances  the 
distinction  between  a  symptomatic  athetosis  and  a  pri- 
mary athetosis  may  be  exceedingly  difficult  or  impossible. 
Hence  it  is  not  difficult  to  understand  that  from  time  to 
time  cases  of  what  are  evidently  symptomatic  athetosis 
(athetoid  movements)  should  be  described  as  cases  of 
primary  athetosis.  This  circumstance,  and  the  fact  that 
a  careful  examination  of  a  supposed  case  of  primary 
athetosis  in  the  light  of  our  present  knowledge  of  infan- 
tile hemiplegia  often  reveals  traces  of  an  old  hemiplegia 
which  ten  years  ago  might  have  been  overlooked,  has 
led  some  observers  to  deny  the  existence  of  a  primary 
athetosis.  But  while  we  have  reason  to  think  that  many 
so-called  cases  of  athetosis  are  of  post-hemiplegic  origin, 
we  are  not  at  present  justified  in  maintaining  that  this  is 
true  of  every  case  which  has  been  described  as  athetosis. 
The  athetoid  movements  are  usually  slow,  and  always 
independent  of  voluntary  motion,  though  they  may  be 
increased  by  it.     Sometimes  the  movements  are  not  slow 


Il8  DISEASES   OF   THE   NERVOUS   SYSTEM. 

but  quick,  and  they  may  then  bear  some  resemblance  to 
chorea.  On  the  strength  of  this  occasional  resemblance 
these  athetoid  movements  have  been  described  as  post- 
hemiplegic chorea,  or  choreatic  paresis — an  objectionable 
term,  because  the  condition  has  nothing  to  do  with  the 
true  chorea. 

As  already  mentioned,  athetoid  movements  are  a 
sequel  to  hemiplegia,  particularly  of  that  which  occurs 
in  childhood.  The  lesion  is  usually  meningeal  hemor- 
rhage or  venous  thrombosis;  sometimes  it  is  embolism, 
sometimes  hemorrhage.  In  adults  the  disease  may  suc- 
ceed cerebral  hemorrhage  or  softening  from  any  cause. 
In  general,  the  movements  are  more  likely  to  follow 
cerebral  softening  than  hemorrhage.  As  regards  the 
position  of  the  lesion  which  underlies  these  athetoid 
movements  or  choreatic  paresis,  no  accurate  generaliza- 
tion can  yet  be  made.  Frequently  the  motor  cortex  has 
been  the  seat  of  disease,  and  it  has  been  shown  that  dis- 
ease in  this  situation  is  by  itself  competent  to  occasion 
the  symptom.  Disease  of  the  internal  capsule  may 
cause  the  symptom,  and  involvement  of  the  adjacent 
gray  matter  (optic  thalamus  and  caudate  nucleus)  is 
probably  not  an  essential  condition  for  its  production. 
Any  slight  diffuse  lesion  of  the  motor  path  of  the  brain 
during  development  may  give  origin  to  the  symptom. 

Associated  Movements. — When  a  voluntary  move- 
ment of  one  group  of  muscles  is  accompanied  by  an  in- 
voluntary contraction  of  muscles  in  another  part  of  the 
body  this  is  termed  an  associated  movement.  Associated 
movements  are  met  with  generally  as  the  result  of  hemi- 
plegia, particularly  the  hemiplegia  of  infancy.  Usually 
the  movements  are  confined  to  the  upper  extremity,  the 
fingers  of  the  paralyzed  side  undergoing  involuntary 
movement,  of  limited  range,  during  the  voluntary  activ- 


SYMPTOMATOLOGY   OF  NERVOUS   DISEASES,      II9 

• 

ity  of  the  other  arm.  Sometimes  these  movemerrts  are 
associated  only  with  extensive  movements  of  the  normal 
limb,  and  are  then  themselves  extensive  in  range,  as 
when  the  paralyzed  arm  is  lifted  above  the  head,  when 
the  other  is  employed  in  an  action  which,  like  pulling 
the  strap  in  a  car,  requires  the  elevation  of  the  arm 
above  the  head.  More  commonly  the  associated  move- 
ments are  narrow  in  range,  and  are  best  seen  when  the 
hand  of  the  unparalyzed  side  is  employed  in  fine  co- 
ordinated movements,  as  in  the  buttoning  or  unbuttoning 
of  the  coat,  or  in  the  fingering  of  any  small  object.  As- 
sociated movements  have  a  significance  similar  to  that  of 
athetoid  movements.  Their  explanation  is  doubtless  to 
be  found  in  the  connection  of  the  subsidiary  centres 
through  which  they  are  produced.  They  possess  little 
diagnostic  importance. 

Inco-ordination. —  During  an  ordinary  muscular 
movement  there  occurs  not  only  an  accurately  propor- 
tioned contraction  of  the  various  muscles  which  produce 
the  movement,  but  a  less  powerful  contraction  of  an- 
tagonistic muscles.  This  adjustment  of  opposed  muscles 
makes  the  movement  which  results  from  their  activity 
regular  and  continuous.  If  the  contraction  of  muscles 
in  either  group  is  excessive,  or  less  than  normal,  the 
movement  which  results  is  not  that  intended,  but  is 
irregular  and  broken,  and  efforts  to  remedy  it  are  often 
excessive  in  degree  and  increase  the  difficulty.  The 
condition  of  irregular,  inco-ordinated  voluntary  move- 
ment is  termed  ataxia.  It  is  difficult  to  say  just  what 
defects  of  co-ordination  the  term  ataxia  should  include; 
whether  it  should  be  applied  to  all  forms  of  inco-ordina- 
tion, or  whether  it  should  be  strictly  limited  to  that  form 
of  inco-ordination  in  which  there  is  loss  of  harmony  in 
the  various  muscle-groups  used  in  the  purely  voluntary 


I20         DISEASES   OF   THE   NERVOUS   SYSTEM. 

execution  of  particular  acts  and  in  which  an  effort  to 
correct  the  defect  only  serves  to  increase  it.  We  shall 
employ  the  term  in  this  restricted  sense.  Under  this 
definition  ataxia  does  not  include  jerky  inco-ordination 
or  ataxic  tremor  such  as  is  seen  in  multiple  sclerosis  and 
general  paralysis,  nor  mere  uncertainty  in  voluntary 
movements,  nor  the  staggering  which  results  from  de- 
fective equilibration. 

According  to  the  position  of  the  lesion  in  the  nervous 
system  it  is  customary  to  distinguish  several  varieties  of 
ataxia.  Thus  there  are  described  a  cortical  ataxia,  a  cere- 
bellar ataxia,  a  bulbar  ataxia,  a  spinal  ataxia,  and  an 
ataxia  from  peripheral  nerve  disease.  Probably  all  are 
cortical  in  their  primary  origin.  Some  of  these  regional 
forms,  however,  are  not  ataxias,  strictly  speaking,  and 
we  shall  therefore  speak  of  them  as  varieties  of  inco- 
ordination, specifying  which  are  true  ataxias. 

Cortical  Inco-ordination. — Inco-ordination  of  movement 
from  cortical  lesions  is  usually  associated  with  paralysis 
of  the  same  distribution.  The  inco-ordination  which  is 
observed  in  athetoid  movements  (so-called  post-hemi- 
plegic  chorea)  has  been  mentioned.  In  cases  of  infantile 
hemiplegia,  however,  inco-ordination  may  be  developed 
only  during  voluntary  movement  and  be  of  a  jerky,  oscil- 
latory character, deserving  the  name  of  ataxia  (hemiataxia 
it  is  called,  when  due  to  a  unilateral  lesion).  Sometimes 
it  is  difficult  to  say  whether  we  should  class  a  given  form 
of  post-hemiplegic  inco-ordination  as  an  active  tremor  or 
as  a  true  ataxia.  The  same  difficulty  is  met  in  the  inco- 
ordination of  dementia  paralytica,  which  is  sometimes 
truly  ataxic,  but  more  generally  consists  of  movements 
of  narrow  range  which  are  more  properly  designated 
tremor. 

The    disturbances    of    co-ordination    which   occur   in 


SYMPTOxMATOLOGY    OF   NERVOUS   DISEASES.      121 

hysteria  are  probably  of  cortical  origin.  They  may  exist 
alone  or  be  accompanied  with  loss  of  power  or  anaesthe- 
sia. It  is  doubtful  whether  the  movements  are  ever 
those  of  true  ataxia.  In  one  form  movements  are  well 
controlled  and  regular  while  the  eyes  are  directing  them, 
but  when  the  visual  control  is  withdrawn  they  become 
grossly  irregular.  In  other  cases  there  is  good  co- 
ordination while  the  patient  lies  in  the  horizontal  posi- 
tion, but  in  standing  she  begins  to  sway  from  side  to 
side.  Again  hysterical  patients  in  whom  there  is  no  loss 
of  cutaneous  or  muscular  sensibility,  though  quite  steady 
with  the  eyes  open,  may  oscillate  from  side  to  side  or 
even  fall  when  the  eyes  are  closed.  The  term  "  astasia  " 
is  sometimes  used  to  designate  the  unsteadiness  in  stand- 
ing, with  or  without  visual  guidance,  that  is  seen  in 
some  cases  of  hysteria.  The  word  "  abasia  "  is  used  to 
designate  the  unsteadiness  in  walking,  which  often  does 
not  amount  to  inco-ordination,  seen  in  the  same  class  of 
cases. 

The  effect  of  withdrawing  the  visual  guidance  in  these 
cases  is  greater  than  it  ever  is  in  true  ataxia  without  de- 
fective sensibility.  This  latter  form  of  inco-ordination 
may  be  of  considerable  diagnostic  value,  since  it  may 
exist  when  other  marked  evidences  of  hysteria  are  absent. 

Why  ataxia  sometimes  occurs  in  cortical  disease  but 
more  frequently  does  not  occur,  it  is  impossible  at  pre- 
sent to  say.  Sometimes  it  seems  to  be  due  to  damage 
of  the  cortical  centre  for  the  muscular  sense  (superior 
parietal  lobule),  sometimes  to  the  disturbance  of  cu- 
taneous sensibility  which  the  lesion  produces.  The 
inco-ordination  seen  in  alcoholic  and  other  forms  of 
intoxication  is  probably  in  part  cortical. 

Cerebellar  Inco-ordination  {^cerebellar  titubatiori) . — This 
form  of  motor  disturbance  consists  in   an  inability  to 


122    ,     DISEASES   OF  THE   NERVOUS   SYSTEM. 

maintain  the  erect  position  or  to  walk  straight,  in  conse- 
quence of  deficient  equilibrium.  The  patient,  in  order 
to  increase  his  base  of  support,  stands  with  the  feet 
apart.  The  body  is  bent  forward  and  the  arms  aie  used 
to  help  in  the  maintenance  of  the  equilibrium,  but  there 
is  no  true  ataxia,  although  the  condition  is  often  called 
cerebellar  ataxia.  The  forefinger  can  be  placed  on  the 
nose  without  difficulty,  and  if  the  patient  is  supine,  there 
is  no  difficulty  in  moving  the  lower  extremities  as  desired. 
The  disorder  is  chiefly  one  of  defective  equilibration  and 
the  gait  frequently  is  much  like  that  seen  in  intoxication 
from  alcohol.  Rarely  the  upper  extremities  present 
marked  jerky  inco-ordination.  This  symptom  is  gener- 
ally due  to  damage  of  the  middle  lobe  of  the  cerebellum, 
sometimes  to  disease  in  it,  sometimes  to  pressure  upon  it 
from  disease  of  one  of  the  cerebellar  hemispheres.  Dis- 
ease of  the  cerebellar  hemispheres  is/<?r  se  not  productive 
of  cerebellar  inco-ordination;  but  wild  inco-ordinated 
movements,  resembling  those  of  cerebellar  titubation, 
may  result  from  pontine  and  medullary  disease,  probably 
from  damage  to  the  sensory  tract  (fillet).  A  peculiar 
difficulty  in  maintaining  the  equilibrium  in  the  act  of 
walking  is  sometimes  seen  in  paralysis  agitans,  and  may 
bear  some  res.emblance  to  cerebellar  titubation.  As  the 
patient  tries  to  walk,  the  first  steps  may  be  taken  with 
difficulty  and  slowly,  but  they  gradually  increase  in 
rapidity  and  soon  the  patient  may  appear  about  to  run 
in  a  staggering  way.  This  tendency  to  run  is  termed 
"festination. ' '  The  body  often  inclines  forward,  and  the 
patient  may  seem  to  be  about  to  fall  as  he  staggers  for- 
ward— "propulsion"  the  tendency  is  called  when 
marked.  More  rarely  it  is  easier  for  the  patient  to  walk 
backwards  than  forwards,  and  there  then  exists  an  un- 
avoidable inclination  to  fall  backwards;  this  is  termed 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      I23 

*'  retropulsion.  "  Lateral  pulsion  may  also  occur.  The 
occurrence  of  festination  has  been  accounted  for  on  the 
supposition  that  the  forward  inclination  of  the  body  and 
head  makes  the  patient  run  after  his  centre  of  gravity, 
but  this  is  certainly  not  the  entire  explanation,  for  retro- 
pulsion, which  doubtless  has  a  similar  mechanism^  may 
occur  though  the  head  and  body  still  incline  forward. 

Bulbar  Inco- ordination.  —  Occasionally  inco-ordmation 
is  met  with  as  a  result  of  disease  of  the  medulla  involving 
the  fillet  (see  page  60),  which  is  probably  one  path  for 
sensory  impressions  from  the  muscles.  This  is  an  un- 
usual cause  of  inco-ordination.  The  characters  of  bulbar 
inco-ordination  appear  to  be  largely  those  of  the  inco- 
ordination of  spinal-cord  disease. 

Inco-ordination  froJH  Spinal-Cord  Disease . — The  muscu- 
lar inco-ordination  which  constitutes  so  important  a 
symptom  in  certain  forms  of  spinal-cord  disease  is  prob- 
ably of  sensory  origin,  though  it  is  usually  classed  with 
motor  symptoms.  The  underlying  cause  of  the  symptom, 
which  in  chronic  disease  of  the  cord  usually  amounts  to 
ataxia,  is  in  the  majority  of  instances  disease  of  the 
posterior  columns  of  the  cord,  especially  the  posterior 
median  column,  occurring  alone  or  in  combination  with 
disease  of  the  posterior  nerve-roots.  Disease  of  the 
posterior  median  columns,  containing,  as  we  have  seen 
(page  60)  one  of  the  paths  for  muscular  sensibility,  is 
probably  operative  in  the  production  of  inco-ordination 
by  the  arrest  of  the  upward  conduction  of  impressions 
from  the  muscles  to  the  cerebellum.  The  impressions 
thus  carried  are  probably  an  important  factor  in  cerebel- 
lar co-ordination,  and  it  is  not  difficult  to  conceive  how 
interruption  of  this  path  may  bring  about  disturbance  of 
co-ordination.  In  the  condition  known  as  ataxic  para- 
plegia this  is  the  probable  mechanism  of  the  ataxia  that 


124         DISEASES   OF   THE   NERVOUS   SYSTEM. 

is  observed.  In  cases  of  unilateral  lesion  of  the  cord, 
also,  loss  of  the  sense  of  posture,  followed  by  ataxia,  has 
been  observed.  This  ataxia  is  referable  to  arrest  of 
sensory  conduction  from  the  muscles,  and  not  to  anaes- 
thesia, for  the  ataxia  is  on  the  same  side  as  the  lesion, 
while  the  cutaneous  anaesthesia  is  on  the  opposite  side, 
and  the  ataxic  muscles  have  been  known  to  lose  their 
sensitiveness  to  pressure.  The  injury  to  the  direct 
cerebellar  tract,  one  of  the  paths  of  muscular  sensibility, 
which  occurs  in  these  cases  of  unilateral  lesion,  may 
also  be  a  factor  in  the  production  of  the  ataxia. 

But  the  mechanism  of  inco-ordination  in  spinal-cord 
disease  is  not  always  so  simple,  for  in  ataxia  in  its  most 
typical  form  there  occurs  an  almost  constant  process  of 
disease  in  the  posterior  nerve-roots  and  often  there  is 
also  disease  of  the  sensory  peripheral  nerve-fibres. 
Among  other  effects  resulting  from  the  involvement  of 
these  structures  is  cutaneous  anaesthesia,  which  though 
not  an  absolutely  constant  condition  is  rarely  entirely 
absent.  This  cutaneous  anaesthesia  has  been  regarded 
by  some  as  a  very  important  factor  in  the  production 
of  ataxia.  But  it  is  highly  probable  that  while  cutaneous 
anaesthesia  may  be  an  accessory  cause  of  ataxia  it  cannot 
operate  as  a  primary  cause.  It  has  been  shown  that 
there  is  no  definite  relation  between  the  degree  of  inco- 
ordination and  the  degree  or  extent  of  the  anaesthesia  in 
conditions  where  both  are  present,  and  it  is  not  rare  to 
meet  with  absolute  and  extensive  anaesthesia  without  the 
least  ataxia,  while  on  the  other  hand,  there  are  cases  in 
which  there  is  marked  ataxia  without  anaesthesia.  Yet 
there  is  good  reason  to  believe  that  anaesthesia  may  in- 
crease pre-existing  ataxia,  and  it  probably  does  so  by 
withdrawing  the  guidance  to  the  motor  cerebral  centres 
which   the   ordinary  cutaneous   impressions   continually 


SYMPTOMATOLOGY    OF   NERVOUS   DISEASES.      I25 

furnish.  It  is  interesting  to  note  in  this  connection  that 
visual  impressions  give  similar  guidance  and  that  the 
withdrawal  of  this  aid  by  closure  of  the  eyes  always  in- 
creases pre-existing  inco-ordination.  We  may  therefore 
regard  anaesthesia  as  an  element  in  the  production  of 
inco-ordination  of  locomotor  ataxia.  As  in  ataxic  para- 
plegia, the  primary  factor  is  usually  the  interruption  of 
impressions  from  the  muscles  to  the  cerebellum  conse- 
quent upon  sclerosis  of  the  postero-median  columns  or 
more  precisely  disease  of  the  afferent  muscle  nerves. 
We  shall  presently  see  that  disease  of  the  sensory  periph- 
eral nerves  is  competent  to  give  rise  to  inco-ordination 
and  such  disease  is  always  encountered  in  locomotor 
ataxia.  We  must  therefore  admit  that  this  factor  is  the 
essential  one  for  the  ataxia  of  tabes. 

Inco-ordination  from  Disease  of  Peripheral  JVerves. — 
Inco-ordination  of  movement  may  occur  from  disease 
involving  exclusively  the  peripheral  nerves.  It  may  be 
dependent  in  part  upon  the  resulting  anaesthesia  as  just 
explained,  but  the  important  factor  is  probably  the  inter- 
ruption of  impressions  from  the  muscles  to  the  cerebel- 
lum, the  result  of  disease  of  the  sensory  muscle  nerves. 
The  process  may  involve  the  sensory  nerves  throughout 
their  extent,  from  the  muscles  to  the  cord,  or  may  in- 
volve them  in  a  limited  part  only  of  their  extent,  for  ex- 
ample at  the  posterior  nerve-roots  as  in  locomotor  ataxia. 
Inco-ordination  of  similar  origin  is  seen  in  alcoholic, 
diphtheritic,  and  some  rarer  forms  of  multiple  neuritis. 
In  the  alcoholic  form  the  inco-ordination  is  sometimes 
indistinguishable  from  that  of  tabes. 

The  sense  of  posture  is  undoubtedly  derived  in  great 
part  from  the  stimulation  of  the  sensory  muscle-nerves 
by  muscular  contraction  and  tension,  but  it  is  probable 
that   nerve   filaments    supplying  adjacent  joint-surfaces 


126         DISEASES   OF  THE   NERVOUS   SYSTEM. 

play  a  role  in  the  recognition  of  posture  by  centripetal, 
transmission  of  impressions  from  the  apposition  of  joint- 
surfaces  at  different  parts,  according  to  the  position  of 
the  segments  above  and  below  the  joint.  These  sensory 
impressions  probably  help  in  the  co-ordination  of  mus- 
cular movements,  and  their  interruption  may  lead  to 
some  disturbance  of  co-ordination,  but  how  far  this 
mechanism  may  be  effective  we  do  not  yet  know. 

Certain  symptoms  referable  directly  or  indirectly  to 
the  ocular  muscles  may  be  conveniently  considered  here. 
These  are  conjugate  deviation,  strabismus,  diplopia,  nys- 
tagmus, and  ptosis. 

Conjugate  Deviation  of  the  Eyes  and  Head. — 
In  many  cases  of  brain  disease  there  is  a  lateral  move- 
ment of  the  eyes  (by  the  external  rectus  of  one  side  and 
the  internal  rectus  of  the  other)  and  often  a  rotation  of 
the  head  (chiefly  by  the  opposite  sterno-mastoid)  toward 
one  or  other  side.  This  is  known  as  conjugate  deviation. 
The  axes  of  the  eyes  are  always  parallel  in  conjugate 
deviation,  whatever  may  be  their  direction. 

Conjugate  deviation  occurs  most  often  as  an  accom- 
paniment of  hemiplegia,  whatever  may  be  its  cause,  and 
may  occur  when  the  lesion  is  in  the  cortex  (probably  the 
posterior  part  of  the  second  frontal  convolution),  in  the 
subcortical  white  substance,  in  the  internal  capsule,  or 
in  the  pons.  The  symptom  may  depend  on  a  destruc- 
tive process  (paralytic  conjugate  deviation)  or  on  an 
irritative  process  (spasmodic  conjugate  deviation).  In 
the  former  case  the  deviation  is  to  the  side  of  the  lesion; 
the  patient  is  said  to  "  look  at  his  lesion."  In  the  latter 
case  the  deviation  is  to  the  side  opposite  the  lesion — that 
is,  to  the  paralyzed  side.  Spasmodic  conjugate  devia- 
tion is  generally  transient.  It  is  often  present  for  a  short 
time  after  acute  hemiplegias,  and  is  not  rarely  seen  in 


SYMPTOMATOLOGY    OF   NERVOUS   DISEASES.      12/ 

acute  meningitis.  The  spasmodic  form  also  occurs  in 
some  cases  of  uraemia,  generally  associated  with  convul- 
sions. It  then  depends  on  cortical  irritation  by  morbid 
blood  products. 

In  cases  where  conjugate  deviation  occurs  the  asso- 
ciated condition  of  the  limbs  shows  whether  the  symptom 
is  paralytic  or  spasmodic  in  origin. 

In  some  cases  of  disease  of  the  pons  there  occurs  a 
peculiar  form  of  associated  paralysis  of  the  external  rec- 
tus of  one  side  with  the  internal  rectus  of  the  other,  in 
which  the  eyes  can  be  turned  towards  the  lesion  to  the 
middle  line,  but  not  beyond  it. 

Strabismus. — Strabismus  is  loss  of  parallelism  in  the 
visual  axes  of  the  two  eyes.  This  loss  of  parallelism  is 
a  conspicuous  symptom  of  many  cases  of  paralysis  of  the 
ocular  muscles.  But  strabismus  is  not  always  of  para- 
lytic origin;  it  may  depend  on  spasm  of  ocular  muscles. 
Spasmodic  strabismus  is  usually  transient,  with  one  ex- 
ception— the  ordinary  form  of  squint  (due  most  often  to 
myopia),  in  which  it  is  persistent. 

In  cases  of  strabismus  dependent  on  paralysis  there 
occurs  what  is  known  as  *'  secondary  deviation."  Pri- 
mary deviation  is  the  deviation  of  the  axis  of  the  eye 
paralyzed,  from  parallelism  with  that  of  the  normal  eye. 
Secondary  deviation  is  something  quite  different.  It  is 
an  excessive  movement  on  the  part  of  the  sound  eye, 
Vhich  increases  the  deviation  from  parallelism,  when  the 
sound  eye  is  prevented  (as  by  interposing  the  hand  or  a 
piece  of  ground  glass)  from  seeing  an  object  looked  at 
with  the  eye  paralyzed. 

By  means  of  this  secondary  deviation  it  is  possible  to 
distinguish  between  paralytic  and  spasmodic  strabismus, 
for  secondary  deviation  always  occurs  in  paralytic,  never 
in  spasmodic  strabismus.     Spasmodic  strabismus  is  the 


128         DISEASES   OF   THE   NERVOUS   SYSTEM. 

same  in  all  positions  of  the  eyes;  paralytic  strabismus 
occurs  only  in  those  positions  of  the  eyes  that  necessitate 
the  use  of  the  muscle  or  muscles  affected. 

Strabismus  may  be  divergent  (external  strabismus)  or 
convergent  (internal  strabismus)  or  may  cause  a  differ- 
ence in  the  level  of  the  two  eyes. 

Transient  spasmodic  strabismus  is  not  rarely  seen  in 
irritative  brain  diseases,  as  meningitis,  tumor,  abscess, 
hemorrhage,  or  softening,  and  occasionally  occurs  in 
hysteria. 

Diplopia. — Double  vision  is  present  in  all  recent 
cases  of  strabismus,  and  is  due  to  the  erroneous  projec- 
tion of  the  field  of  vision  of  the  affected  eye.  When  the 
strabismus  is  of  long  duration  (whatever  may  be  the 
cause)  the  patient  learns  to  disregard  the  image  formed 
on  the  retina  of  the  affected  eye  ("  false  image  "),  and 
he  then  becomes  aware  only  of  those  things  that  are  seen 
with  the  normal  eye.  In  such  chronic  cases  the  false 
image  may  be  brought  out  by  placing  a  bit  of  colored 
glass  before  one  eye  (preferably  the  sound  eye)  in  order 
to  color  either  the  true  or  false  image  (the  true  image  in 
the  case  of  the  normal  eye). 

Double  vision  is  often  an  early  symptom  of  brain  dis- 
ease, as  meningitis,  tumor,  abscess,  multiple  sclerosis. 
In  many  cases  it  accompanies  the  onset  of  sudden  lesions, 
especially  those  in  or  near  the  pons.  It  depends  here  on 
spasmodic  strabismus,  but  this  is  of  such  duration  as  to* 
be  unrecognized.  The  occurrence  of  diplopia  in  children 
who  are  free  from  eye  disease  (errors  of  refraction)  is 
suggestive  of  meningitis.  When  not  dependent  on  eye 
disease  diplopia  is  usually  a  sign  of  serious  nervous  dis- 
ease, but  this  is  not  always  the  case.  It  occurs,  for 
example,  as  a  transient  symptom  in  many  cases  of  acute 


SYMPTOMATOLOGY    OF   NERVOUS   DISEASES.      1 29 

alcoholism  and  certain  drug  intoxications  and  in  some 
cases  of  cerebral  concussion. 

Nystagmus  is  the  term  applied  to  rapid  involuntary 
and  rhythmical  movements  of  the  eyes.  The  movements 
are  usually  bilateral  and  similar  in  character  in  both 
eyes.  Most  often  the  movements  are  horizontal;  some- 
times they  are  rotary;  rarely  they  are  vertical.  They 
vary  in  frequency  from  60  to  200  movements  per  minute 
in  the  same  direction.  All  forms  cease  during  sleep. 
Usually  the  rhythm  of  movement  is  regular. 

Nystagmus  is  usually  constant.  Occasionally  it  occurs 
only  when  the  eyes  are  moved  in  certain  directions. 
Often  it  persists  in  central  fixation.  In  cases  that  date 
from  early  life,  the  patients  are  not  congcious  of  the 
movement  of  their  eyes;  but  in  some  cases  that  begin  in 
adult  life  there  is  apparent  movement  of  objects  at  least 
for  a  time. 

Nystagmus  is  observed  in  a  number  of  different  condi- 
tions. It  occurs  (a)  from  conditions  external  to  the 
nervous  system,  and  (^)  in  many  different  diseases  of 
the  nervous  system.  Of  the  conditions  external  to  the 
nervous  system  that  cause  nystagmus,  the  following  are 
the  chief:  albinism,  a  very  common  cause,  and  local  eye 
affections  causing  defective  sight,  as  opacities  of  the 
cornea  or  lens  and  diseases  of  the  choroid  or  retina 
(effective  chiefly  in  childhood).  It  is  also  of  frequent 
occurrence  in  miners  who  work  in  coal  mines  in  a  dim 
light  in  postures  that  require  excessive  tension  in  certain 
eye  muscles  for  a  long  time. 

Of  the  diseases  of  the  nervous  system  in  which  nystag- 
mus occurs  the  most  important  are  these:  multiple 
sclerosis,  hereditary  ataxia,  meningitis,  meningeal  hemor- 
rhage, and  cases  of  tumor,  and  hemorrhage  and  softening 


130         DISEASES   OF  THE  NERVOUS   SYSTEM. 

in  almost  any  situation.  Cerebellar  disease  (especially 
tiimor)  is  often  associated  with  nystagmus,  and  pontine 
disease  is  occasionally  the  apparent  cause  of  nystagmus. 
In  chronic  ear  disease  and  in  mastoid  disease  nystagmus 
is  sometimes  developed,  in  association  usually  with  symp- 
toms indicating  irritation  of  the  adjacent  membranes. 
Severe  cerebral  concussion  is  sometimes  followed  imme- 
diately by  nystagmus  (the  oscillations  may  be  very  rapid) 
of  temporary  duration,  and  may  depend  in  these  cases 
on  minute  hemorrhages  into  the  brain  substance.  Nys- 
tagmus is  occasionally  observed  in  the  course  of  ursemic 
convulsions  and  exhaustion   of  status  epilepticus. 

The  mechanism  and  significance  of  nystagmus  are  but 
imperfectly  understood.  It  is  certainly  central  in  origin 
and  probably  due  to  a  disarrangement  of  function  of  the 
third  nerve  nuclei  of  the  two  sides  or  their  connection 
with  centres  of  equilibration.  The  symptom  certainly 
has  little  or  no  localizing  value,  for  it  arises  from  dis- 
ease in  a  great  variety  of  positions  in  the  brain.  It  is, 
however,  an  important  symptom,  for  it  usually  indicates 
more  than  purely  functional  disorder,  especially  when 
associated  with  other  evidence  of  nervous  disease. 

When  it  develops  gradually  in  adults  as  the  result  of 
nervous  disease  this  is  most  often  degenerative  in  nature. 

Ptosis,  or  drooping  of  the  eyelid,  is  a  symptom  of 
several  distinct  conditions.  Most  often  it  is  the  result  of 
disease  of  the  third  nerve  (generally  syphilitic  disease), 
and  is  then  associated  with  other  symptoms.  But  it  may 
result  from  disease  of  the  third  nerve  nucleus,  or  of  the 
tract  of  the  third  nerve  anywhere  between  the  nucleus 
and  the  cortical  centre.  (The  position  of  the  cortical 
centre  is  uncertain  ;  perhaps  it  is  in  the  lower  parietal 
lobule.)  Generally,  ptosis  from  disease  o^  the  third  nerve 
tract  is  unilateral,  but  in  some  cases  of  nuclear  disease 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      I31 

and    disease     of    the     nerve    itself    the    symptom    is 
bilateral. 

Ptosis  from  paralysis  of  the  sympathetic  is  occasionally 
seen,  and  is  distinguished  by  other  evidences  of  sympa- 
thetic involvement,  especially  contraction  of  the  pupil  on 
the  same  side.  In  these  cases  the  drooping  of  the  lid 
probably  depends  on  paralysis  of  the  smooth  muscular 
fibres  of  the  fascia  of  the  orbit  (fibres  of  Mtiller),  which 
are  supplied  by  the  sympathetic,  and  normally  act  on  the 
tarsal  cartilages. 

Some  cases  (usually  bilateral  and  partial)  of  ptosis  are 
congenital,  and  ignorance  of  this  fact  may  lead  to  errors 
in  diagnosis.  Hysterical  ptosis  is  sometimes  seen,  and 
may  be  bilateral  or  single.  It  is  generally  associated  with 
spasm  of  the  orbicularis. 

Reflex  ptosis,  a  rare  form,  generally  depends  on  some 
morbid  state  (irritative  usually)  of  the  fifth  nerve,  as 
extraction  of  a  tooth,  or  injury  of  the  nerve.  In  some 
neurasthenics  ptosis  develops  in  middle  life.  It  is  always 
double.  "  Morning  ptosis  "  is  a  form  in  which  the  patient, 
on  waking,  is  temporarily  unable  to  lift  the  lid.  Ptosis 
also  occurs  in  the  relapsing  and  recurring  palsies  of  the 
third  nerves.  Some  other  forms  of  ptosis  are  associated 
with  over-action  of  the  occipito-frontalis. 

Pupillary  Symptoms. — Deviations  from  the  normal 
reaction  and  size  of  the  pupils  are  of  frequent  occurrence 
in  disease  of  the  nervous  system,  and  possess  considerable 
diagnostic  importance.  The  most  important  of  these 
deviations  are  the  following  : 

(1)  Dilatation  of  the  Pupils  with  normal  reactions 
to  light  and  during  accommodation.  Such  dilatation  is 
often  observed  in  children  and  in  nervous  and  irritable 
adults  in  apparently  good  health.  It  is  frequently  seen 
in  neurasthenic,  hysterical,   and  maniacal    persons,  and 


. »»«wr>©\ 


130 


DISEASES   OF  THE  NERVOUS   SYSTEM. 


in  almost  any  situation.  Cerebellar  disease  (especially 
tumor)  is  often  associated  with  nystagmus,  and  pontine 
disease  is  occasionally  the  apparent  cause  of  nystagmus. 
In  chronic  ear  disease  and  in  mastoid  disease  nystagmus 
is  sometimes  developed,  in  association  usually  with  symp- 
toms indicating  irritation  of  the  adjacent  membranes. 
Severe  cerebral  concussion  is  sometimes  followed  imme- 
diately by  nystagmus  (the  oscillations  may  be  very  rapid) 
of  temporary  duration,  and  may  depend  in  these  cases 
on  minute  hemorrhages  into  the  brain  substance.  Nys- 
tagmus is  occasionally  observed  in  the  course  of  uraemic 
convulsions  and  exhaustion   of  status  epilepticus. 

The  mechanism  and  significance  of  nystagmus  are  but 
imperfectly  understood.  It  is  certainly  central  in  origin 
and  probably  due  to  a  disarrangement  of  function  of  the 
third  nerve  nuclei  of  the  two  sides  or  their  connection 
with  centres  of  equilibration.  The  symptom  certainly 
has  little  or  no  localizing  value,  for  it  arises  from  dis- 
ease in  a  great  variety  of  positions  in  the  brain.  It  is, 
however,  an  important  symptom,  for  it  usually  indicates 
more  than  purely  functional  disorder,  especially  when 
associated  with  other  evidence  of  nervous  disease. 

When  it  develops  gradually  in  adults  as  the  result  of 
nervous  disease  this  is  most  often  degenerative  in  nature. 

Ptosis,  or  drooping  of  the  eyelid,  is  a  symptom  of 
several  distinct  conditions.  Most  often  it  is  the  result  of 
disease  of  the  third  nerve  (generally  syphilitic  disease), 
and  is  then  associated  with  other  symptoms.  But  it  may 
result  from  disease  of  the  third  nerve  nucleus,  or  of  the 
tract  of  the  third  nerve  anywhere  between  the  nucleus 
and  the  cortical  centre.  (The  position  of  the  cortical 
centre  is  uncertain  ;  perhaps  it  is  in  the  lower  parietal 
lobule.)  Generally,  ptosis  from  disease  o^  the  third  nerve 
tract  is  unilateral,  but  in  some  cases  of  nuclear  disease 


.„ 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      133 

disease)  of  the  brain,  which  interrupts  the  reflex  path 
between  the  optic  nerve  and  the  nucleus  of  the  third 
nerve.  The  Argyll-Robertson  pupil  is  a  characteristic 
symptom  of  locomotor  ataxia  and  of  general  paresis, 
and  is  an  occasional  symptom  of  multiple  sclerosis.  In 
rare  cases  it  is  observed  in  persons  who  have  syphilis 
but  have  no  signs  of  organic  brain  disease.  The  Argyll- 
Robertson  pupil  is  usually  associated  with  contraction 
of  the  pupil ;  occasionally  with  dilatation,  or  with  pupils 
of  normal  or  unequal  size. 

(5)  Mere  Difference  in  the  Size  of  the  Pupils  has  no 
single  significance.  Such  difference  is  common  in  cases 
where  the  two  eyes  refract  differently.  A  high  grade  of 
inequality  is  sometimes  seen  when  there  is  little  defect 
in  vision.  Inequality  is  often  observed  in  irritative  dis- 
eases of  the  brain — meningitis,  abscess,  tumor,  extra- 
dural hemorrhage,  etc.,  and  in  degenerative  diseases, 
such  as  locomotor  ataxia  and  dementia  paralytica — but  is 
seldom  of  more  than  secondary  importance  in  diagnosis. 

Changes  in  the  size  and  reaction  of  the  pupils  from 
nervous  diseases  are  readily  distinguishable  from  the 
changes  in  size  and  immobility  that  depend  on  iritic 
adhesions.  The  immobile  pupils  of  iritis  are  almost 
always  irregular  in  form,  and  proper  illumination  will 
reveal  the  presence  of  synechiae. 

(6)  Hemianopic  Pupillary  Inaction. — This  term  is  ap- 
plied to  the  imperfect  reaction  which  occurs  when  light 
is  thrown  on  the  blind  half  of  the  retina  in  certain  cases 
of  hemianopsia.  The  cases  of  hemianopsia  in  which 
pupillary  reaction  is  diminished  or  lost  when  the  blind 
half-field  is  stimulated,  are  those  in  which  the  lesion  is  in 
the  optic  tract ;  the  cause  of  the  phenomena  being  the 
interruption  of  the  path  to  the  corpora  quadrigemina  (or 
ganglion  habenulae).      In  cases   of  hemianopsia  due  to 


134         DISEASES   OF   THE   NERVOUS   SYSTEM. 

lesions  of  the  hemisphere  the  hemianopic  pupillary  inac- 
tion does  not  occur.  Hence  the  symptom,  if  carefully 
determined,  is  of  value  in  distinguishing  between  lesions 
of  the  tract  and  those  of  the  intra-cerebral  optic  path 
and  centres. 

Laryngeal  Symptoms. — Disordered  action  of  the 
larynx,  the  organ  of  voice,  may  give  rise  to  important 
symptoms  and  signs.  Of  these  symptoms  the  chief  are  : 
(i)  altered  phonation,  or  entire  loss  of  voice  :  (2)  res- 
piratory symptoms,  as  stridor  and  dyspnoea,  from  imper- 
fect regulation  of  entrance  of  air  in  breathing,  or  cough 
from  imperfect  closure  of  the  glottis.  The  signs  of 
laryngeal  disorder  consist  chiefly  of  defective  movement 
of  the  vocal  cords,  which  may  be  observed  by  means  of 
the  laryngoscope. 

It  is  convenient  to  consider  the  grouping  of  these 
symptoms  and  signs  in  the  various  forms  of  laryngeal 
disorder  (especially  paralysis)  that  are  met  with  as  the 
result  of  nervous  disease. 

(i)  In  Total  Bilateral  Paralysis  of  the  larynx  (or  what 
is  more  common,  paralysis  of  all  the  laryngeal  muscles 
except  the  crico-thyroid)  the  vocal  cords  are  in  the 
"cadaveric  position" — that  is,  in  a  state  of  slight  ab- 
duction from  the  median  line,  and  cannot  be  moved. 
When  an  attempt  at  phonation  is  made  the  cords  can- 
not be  approximated  ;  hence  there  is  loss  of  voice. 
There  is  also  inability  to  make  a  natural  explosive  cough 
— a  symptom  of  much  importance  and  one  which 
always  indicates  laryngeal  paralysis,  usually  organic  in 
character.  There  may  be  stridor  during  deep  in- 
spiration. 

(2)  In  Total  Unilateral  Paralysis  of  the  Larynx  the  para- 
lyzed cord  lies  motionless  in  the  "cadaveric  position." 
The  unparalyzed  cord   moves  freely  and  may  even  pass 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      I35 

beyond  the  median  line  of  the  glottis  during  phonation. 
In  consequence  of  this  compensating  action  phonation  is 
possible,  but  the  voice  is  hoarse  and  low  in  pitch.  There 
is  no  stridor,  and  an  explosive  cough  is  impossible. 
Total  unilateral  paralysis  of  the  larynx  may  result  from 
disease  of  the  spinal  accessory  nucleus  or  its  nerve-roots 
by  the  side  of  the  medulla,  or  from  disease  of  the  root  of 
the  pneumogastric.  But  the  most  common  cause  of  uni- 
lateral paralysis,  and  indeed  of  all  laryngeal  paralyses,  is 
disease  of  the  recurrent  laryngeal  nerve.  Aneurism  of 
the  vessels  round  which  the  nerve  passes,  thoracic  tumor, 
enlarged  bronchial  lymph-nodes,  and  enlargements  of  the 
thyroid  are  all  causes  of  pressure  upon  the  nerve.  The 
crico-thyroid  muscle  is  of  course  exempt  in  these  cases, 
but  the  symptoms  are  practically  the  same  as  when  all 
the  muscles  are  involved.  The  causes  of  total  bilateral 
palsy  are  the  same  as  those  of  the  unilateral  form,  acting 
on  both  sides. 

(3)  In  Total  Abductor  Paralysis  of  the  Larynx  (paralysis 
of  the  posterior  crico-arytenoids)  the  cords  lie  close 
together  (much  nearer  than  in  the  position  of  cadaveric 
rigidity),  and  are  not  abducted  during  inspiration.  The 
effect  upon  respiration  is  that  inspiration  is  difficult  and 
accompanied  with  stridor.  There  may  even  be  alarming 
dyspnoea,  with  lividity  of  the  face,  etc.  Expiration  is 
unembarrassed,  cough  is  normal,  and  the  voice  is  little 
changed. 

(4)  In  Unilateral  Abductor  Paralysis  \ht  recession  oi  ih.^ 
unparalyzed  cord  prevents  both  stridor  and  the  dyspnoea 
which  characterizes  the  bilateral  palsy.  Neither  cough 
nor  voice  are  distinctly  affected.  The  symptoms  are 
therefore  chiefly  negative. 

Abductor  paralysis  of  the  larynx  may  be  due  to  local 
palsy,  as  laryngeal  catarrh,  or  to  central  disease.     Some- 


136         DISEASES   OF   THE   NERVOUS   SYSTEM. 

times  it  appears  to  be  due  to  disease  of  the  recurrent 
laryngeal  nerve.  Occasionally  it  occurs  as  an  hysterical 
paralysis,  and  is  then  double. 

(5)  In  Addiutor  Para'ysis  the  vocal  cords  are  separated 
and  cannot  be  brought  together  nearer  than  the  cadaveric 
position,  but  abduction  is  possible  during  deep  inspira- 
tion. The  voice  is  lost,  but  cough  is  usually  perfect, 
because  the  paralysis  is  generally  partial  and  the  cords 
can  be  approximated  during  the  attempt  to  cough, 
though  not  for  phonation.  There  is  no  stridor  and  no 
dyspnoea. 

Adductor  paralysis  is  only  rarely  due  to  organic  disease. 
It  is  most  often  of  hysterical  origin,  and  gives  rise  to  the 
aphonia  of  hysteria.  Occasionally  it  results  from  simple 
catarrhal  laryngitis. 

(6)  Adductor  Spasm  of  the  Larynx  is  a  common  occur- 
rence in  many  laryngeal  diseases.  It  always  depends  on 
a  state  of  abnormal  central  excitability.  Under  favorable 
conditions  of  excitability  in  the  laryngeal  mechanism 
(such  as  are  frequently  present  in  children)  almost  any 
nerve  irritation,  whether  direct,  reflex,  or  central,  may 
determine  a  paroxysm  of  adductor  spasm.  The  parox- 
ysms consist  of  sudden  and  intense  difficulty  in  breathing 
and  loud  stridor,  lasting  only  a  few  minutes. 

In  children  very  slight  nerve  irritation  often  suffices 
to  determine  the  paroxysm.  In  children  with  rickets 
laryngeal  paroxysms  of  peculiar  type,  associated  with 
cardiac  and  vaso-motor  disturbance  and  known  as  "  laryn- 
gismus stridulus,"  are  not  uncommon.  These  paroxysms 
are  related  in  their  pathology  to  the  general  convulsions 
which  may  occur  in  rickets.  Any  irritative  lesion  of  the 
superior  or  inferior  laryngeal  nerve  may  cause  adductor 
spasm,  which  may  be  bilateral  or  unilateral.  Adductor 
spasm  occurs  also  at  the  onset  of  attacks  of  grand  mal, 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      1 37 

causing  the  "  epileptic  cry,"  during  hydrophobia,  and 
occasionally  in  hysteria  and  tetany. 

Abnormal  Reflex  Action. — The  modifications  of 
reflex  action  which  possess  diagnostic  value  may  con- 
veniently be  considered  here. 

Loss  of  Reflex  Action  occurs  whenever  the  reflex  arc 
which  subserves  the  reflex  in  question  is  interrupted.^ 
As  every  reflex  arc  consists  of  a  centripetal  portion  (sen- 
sory nerve),  a  centrifugal  portion  (motor  nerve),  and  a 
central  portion  (motor  ganglion-cell  of  cord),  the  disease 
abolishing  reflex  action  may  be  in  any  one  of  these  three 
positions.  In  v/hich  particular  one  it  lies  in  a  given  case 
is  to  be  determined  by  the  associated  conditions.  If  the 
disease  is  in  the  sensory  path,  there  is  loss  of  sensibility 
as  well  as  of  reflex  ;  if  in  the  peripheral  motor  path,  or  in 
the  motor  centre,  there  is  corresponding  loss  of  motion, 
with  nerve  degeneration  and  atrophy.  This  is  true  both 
of  the  superficial  and  of  the  deep  reflexes,  but  in  the 
case  of  the  former,  it  has  little  diagnostic  value,  while  as 
regards  the  latter  (especially  the  knee-jerk),  it  is  of  diag- 
nostic importance,  for  the  degenerative  atrophy  which 
results  from  implication  of  the  motor  elements  is  readily 
appreciated  in  the  latter  but  not  in  the  former  instance. 

Disease  within  the  reflex  arc  is  not  the  only  cause  of 
arrested  reflex  action,  for  both  superficial  and  deep 
reflexes  may  be  temporarily  arrested  by  irritative  inhibi- 
tion from  above — that  is,  from  irritative  disease  at  any 
level  higher  than  the  motor  ganglion-cells  on  which  the 
reflex  depends.  This  is  the  explanation  of  the  unilateral 
reflex  loss  which  is  frequently  encountered  immediately 
after  hemiplegia,  and  of  the  bilateral  reflex  loss  which  is 
seen  below  the  lesion  for  a  variable  time  after  sudden 

^  The  different  levels  of  the  spinal  cord  upon  which  the  more 
important  reflexes  depend,  are  jriven  on  pages  24  and  25. 


138         DISEASES   OF   THE   NERVOUS   SYSTEM. 

damage  to  the  cord — as  from  fracture  or  dislocation  of 
the  cervical  vertebrae.  Persistent  loss  of  cutaneous  reflex 
(unilateral  or  bilateral)  occasionally  occurs  as  a  result  of 
disease  of  the  hemispheres.  Persistent  loss  of  tendon 
reflex  probably  never  occurs  from  brain  disease,  but 
temporary  loss  of  knee-jerk  occurs  sometimes  in  irritative 
disease  (tumor)  of  the  cerebellum,  and  is  not  uncommon 
in  lesions  which  irritate  the  cortex  of  the  convexity  (con- 
vexity meningitis,  subarachnoid  hemorrhage).  Probably 
this  is  due  to  irritative  inhibition. 

Loss  of  Patellar  Tendon  Reflex  (knee-jerk)  is  of  much 
diagnostic  significance.     The  more  important  conditions 
in  which  it  occurs  may  be  tabulated  as  follows  : 
(A.)  Diseases  of  the  brain  : 

Almost  any  irritative  brain  disease  involving  motor 
structures  (tumor,  meningitis,  abscess,  hemorrhage,  acute 
softening)  ;  loss  usually  unilateral,  always  temporary 
(hours,  days  or  weeks)  ;  in  convexity  meningitis  and 
subarachnoid  hemorrhage  (bilateral)  the  loss  may  be 
bilateral. 
(B.)  Diseases  of  the  spinal  cord  : 

1.  Locomotor  ataxia.  Very  early  and  constant  symp- 
tom ;  bilateral  (in  very  early  stage  may  be  present  on 
one  side) ;  due  to  destruction  of  reflex  arc  by  disease  of 
posterior  nerve-roots  ;  persistent. 

2.  Poliomyelitis  of  lumbar  cord.  Immediate  onset ; 
generally  unilateral,  sometimes  bilateral  ;  due  to  inter- 
ruption of  reflex  arc  by  disease  of  ganglion-cells  of  ante- 
rior horns. 

3.  Any  diffuse  destructive  process  in  lumbar  cord,  as 
transverse  myelitis. 

4.  Spinal  meningitis.  After  stage  of  irritation  ;  due  to 
compression  of  anterior  or  posterior  nerve-roots  by 
exudation. 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      I39 

(C.)   Diseases  of  the  peripheral  nerves  : 

1.  Alcoholic  neuritis.  Loss  usually  occurs  early  ; 
not  absolutely  constant,  for  knee-jerk  may  occasionally 
be  present  throughout  the  disease  when  muscle-nerves 
for  extensors  of  knee  are  not  involved  ;  due  to  inter- 
ruption of  reflex  arc  by  disease  of  sensory  muscle-nerves. 

2.  Diphtheritic  neuritis.  Frequent  loss  when  there  is 
no  subsequent  paralysis  ;  almost  constant  loss  when  there 
is  post-diphtheritic  paralysis  ;  comes  on  about  one  month 
after  onset  of  disease  ;  usually  bilateral,  rarely  unilateral ; 
return  of  knee-jerk  after  variable  period. 

3.  Acute  ascending  paralysis.  Bilateral  and  early  loss 
very  constant ;  usually  persistent,  but  knee-jerk  may 
return. 

4.  Any  severe  lesion  of  anterior  crural  nerve,  sensory 
or  motor  fibres,  or  both.  Immediate  unilateral  loss  of 
knee-jerk. 

Besides  the  conditions  that  have  been  given  as  causes 
of  loss  of  knee-jerk,  there  are  others  whose  mechanism  is 
at  present  obscure.  Thus,  the  knee-jerks  may  be  lost 
during  the  febrile  stage  of  secondary  syphilis  and  in 
severe  forms  of  malarial  fever, — possibly  in  both  instances 
from  slight  neuritis  of  the  sensory  muscle-nerves  on 
which  the  knee-jerk  depends  ;  for  it  is  certain  that  very 
slight  disease  of  these  nerves  may  cause  temporary  loss 
of  myotatic  irritability.  The  knee-jerk  may  be  perma- 
nently lost  in  diabetes  mellitus. 

It  should  be  remembered  that  in  very  rare  instances 
persistent  absence  of  knee-jerk  is  observed  in  persons 
in  good  heal;h.  It  is  claimed  by  some  that  this  is 
not  such  an  uncommon  occurrence,  but  we  believe  that 
if  the  precautions  recommended  on  page  589  be  observed 
in  testing  the  knee-jerk  such  cases  will  be  found  to  be 
very  rare. 


I40         DISEASES   OF   THE   NERVOUS   SYSTEM. 

Thus  it  is  seen  that  loss  of  knee-jerk  is  by  no  means  a 
pathognomonic  symptom.  Its  chief  general  significance 
is  interruption  of  the  reflex  arc  on  which  it  depends. 
The  exact  character  and  seat  of  the  disease  which  is  thus 
operative  must  be  determined  by  the  study  of  other 
symptoms.  But  it  should  not  be  forgotten  that  interrup- 
tion of  the  reflex  arc  is  not  the  only  significance  of  the 
symptom. 

Excess  of  Reflex  Action  is  of  frequent  occurrence  in 
disease  of  the  nervous  system,  and  is  evidence  for  each 
reflex  that  its  arc  is  intact.  Increase  in  cutaneous  reflex 
action  is  of  little  diagnostic  significance,  partly  because 
of  the  variable  character  of  the  different  skin  reflexes  in 
different  normal  individuals,  and  the  consequent  difficulty 
in  determining  what  constitutes  a  pathological  change. 
An  increase  is,  however,  seen  in  conditions  which,  like 
strychnia  poisoning  and  tetanus,  are  characterized  by  an 
increased  irritability  of  reflex  centres  generally,  and  is  an 
inconstant  effect  of  lesions,  which,  like  certain  cerebral 
and  spinal  diseases  involving  the  pyramidal  tract,  diminish 
spinal  inhibition.  In  locomotor  ataxia  the  superficial 
reflexes  are  sometimes  much  increased  early  in  the 
disease,  the  plantar  increase  being  particularly  notice- 
able. As  the  disease  progresses  upwards,  the  increase 
may  be  seen  in  the  abdominal  reflex.  Probably  this 
increase  is  the  effect  of  irritation  in  the  reflex  arc. 

Increase  in  the  activity  of  the  deep  reflexes,  particu- 
larly the  knee-jerk,  is  a  sign  of  considerable  diagnostic 
importance.  It  is  sometimes  due  to  primary  over-action 
of  the  reflex  centres,  as  in  tetanus  and  strychnia  poison- 
ing. Usually  it  depends  on  defective  inhibition  from 
higher  (cerebral)  centres,  and  this  defective  inhibition 
may  be  brought  about  by  organic  or  functional  disease. 
Permanent  exaggeration  of  the  knee-jerk  is  almost  always 


SYMPTOMATOLOGY   OF   NERVOUS    DISEASES.      14I 

consequent  on  degeneration  of  the  pyramidal  tracts.  The 
excess  is  at  first  slight  in  degree  and  increases  gradually. 
Since  the  conditions  that  lead  to  degeneration  of  the 
pyramidal  tracts  are  numerous,  it  is  not  singular  that 
exaggerated  tendon-reflex  is  seen  in  a  variety  of  organic 
processes.  The  following  are  the  main  conditions  in 
which  it  is  observed  : 

1 .  Hemiplegia  from  any  cause ;  tumor,  hemorrhage, 
softening  ;  increase  comes  on  in  about  a  week  ;  especially 
noticeable  on  side  opposite  lesion  ;  may  be  bilateral ; 
regular  symptom,  except  in  slight  cases. 

2.  General  paresis  with  ataxic  paraplegic  symptoms  ; 
common  and  early  symptom  ;  excess  bilateral. 

3.  Transverse  myelitis  above  lumbar  enlargement  ;  bi- 
lateral excess  usually  great. 

4.  Slow  compression  of  the  cord  above  lumbar  enlarge- 
ment, as  from  caries,  tumor,  etc.  Early  and  great  excess 
always  present  ;  may  occur  when  there  is  no  secondary 
degeneration,  and  may  disappear  when  compression  is 
removed. 

5.  Primary  degenerative  diseases  of  the  cord  ;  primary 
lateral  sclerosis  ;  spastic  paraplegia  ;  amyotrophic  lateral 
sclerosis;  disseminated  sclerosis. 

6.  Injuries  of  spinal  cord  ;  hemisection,  complete 
transverse  section  ;  sudden  destruction  at  one  level  above 
lumbar  enlargement  from  fracture  or  dislocation  of  verte- 
brae. When  injury  is  one-sided,  excess  is  unilateral  and 
on  same  side  ;  excess  following  fracture  or  dislocation 
is  preceded  by  complete  loss  of  reflex  if  transverse  de- 
struction is  extensive. 

Bilateral  increase  of   the  knee-jerks  is  seen  in  func- 
"tional  (nutritional)  diseases  ;   in  hysteria,  hypochondri- 
asis, neurasthenia,  epilepsy,  and  in  certain  neuroses  that 
follow  traumatism  (traumatic  neuroses). 


142         DISEASES   OF   THE   NERVOUS   SYSTEM. 

Increase  of  other  tendon  reflexes,  triceps,  and  supin- 
ator longLis,  has  the  same  general  significance  as  increase 
of  patellar  tendon  reflex,  but  is  of  less  practical  diagnos- 
tic value.  Very  active  knee-jerks  are  frequently  seen  in 
perfectly  healthy  persons. 

Ankle  Clonus  ("foot-clonus")  consists  of  a  series  of 
to-and-fro  movements  (flexion  and  extension)  of  the  foot 
at  the  ankle  joint,  which  may  sometimes  be  induced  by 
suddenly  flexing  the  foot  (dorsal  flexion)  on  the  extended 
and  relaxed  leg.  It  may  also  occur  spontaneously  when 
the  patient  sits  with  the  tips  of  the  toes  on  the  ground 
and  the  heel  raised.  The  movements  are  highly  rhythmi- 
cal, and  number  from  six  to  ten  per  second.  The  gen- 
eral significance  of  ankle  clonus  is  that  of  exaggerated 
tendon  reflexes,  but  the  phenomenon  usually  occurs  only 
in  conditions  where  the  knee-jerk  is  very  much  exagger- 
ated, and  true  clonus  is  never  a  symptom  in  functional 
affections. 

Ankle  clonus  is  usually  evidence  of  organic  disease, 
especially  of  degeneration  of  the  pyramidal  tract,  but  it 
is  frequently  very  marked  in  cases  of  compression  of  the 
cord  in  which  secondary  degeneration  has  not  occurred. 
A  spurious,  irregular,  and  varying  clonus  is  also  seen  in 
the  paraplegic  contracture  of  hysteria,  and  in  the  "  trau- 
matic neurosis."  Ankle  clonus  may  be  obtained  in  some 
normal  individuals  after  they  have  stood  on  tiptoe  for 
some  time.  It  is  very  exceptional  to  meet  with  ankle 
clonus  without  exaggeration  of  the  knee-jerks.  But  in 
rare  lesions  in  the  sacral  cord  it  may  be  present  when  knee- 
jerks  are  absent.  Clonus  of  the  rectus  muscle  (rectus 
clonus)  is  sometimes  obtained  by  striking  the  tendon 
just  above  the  patella.  This  condition  is  usually  present 
when  there  is  ankle  clonus,  but  may  occur  unassociated 
with  it. 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      I43 

Sensory  Symptoms  are  of  frequent  occurrence  in 
both  organic  and  functional  disease  of  the  nervous  sys- 
tem, and  of  the  various  forms  that  are  encountered  loss 
of  sensibility  is  the  most  important.  Certain  forms  of 
sensory  loss  possess  important  localizing  significance, 
but  many  forms  are  at  present  of  little  value,  owing  to 
our  imperfect  knowledge  of  the  sensory  paths. 

It  is  important  to  remember  that  sensory  structures 
(especially  fibres)  often  preserve  their  functional  activity 
entirely  or  in  part,  when  damaged  to  a  degree  (for  ex- 
ample by  pressure)  that  in  motor  elements  would  pro- 
duce complete  loss  of  function.  Hence  it  is  that  lesions 
involving  both  motor  and  sensory  structures  frequently 
either  give  rise  to  no  sensory  loss,  or  are  soon  followed 
by  partial  or  complete  recovery  of  sensibility. 

Different  forms  of  sensory  loss  (anaesthesia,  analgesia) 
often  coexist,  but  not  infrequently  certain  forms  are 
present  while  others  are  lost.  It  is  convenient  to  con- 
sider separately  the  different  forms  of  sensory  loss. 

Ancesthesia  (the  word  anaesthesia  is  also  used  in  a 
general  sense  to  include  loss  of  pain  sense),  loss  of  tactile 
sensibility,  is  met  with  in  diseases  of  the  brain,  spinal  cord, 
and  peripheral  nerves,  and  in  some  nutritional  affections 
(hysteria,  traumatic  neuroses).  Certain  types  of  sensory 
loss,  based  on  distribution,  may  be  distinguished. 

Hemiancesthesia,  or  loss  of  tactile  sensibility  involving 
one  lateral  half  of  the  body — face,  trunk,  and  extremities 
of  one  side, — is  invariably  of  central  origin.  The  hemi- 
anaesthesia  may  be  complete  or  partial,  and  may  or  may 
not  be  associated  with  hemiplegia,  which  may  be  of  any 
degree.  When  of  organic  origin,  complete  hemianaes- 
thesia  is  rarely  associated  with  a  high  grade  of  motor 
paralysis  (unilateral).  Loss  of  pain  and  temperature 
senses  may  be  associated  with  hemianaesthesia,  bat  the 
three  forms  of  sensibility  seldom  suffer    equally.     The 


144         DISEASES   OF  THE   NERVOUS   SYSTEM. 

anaesthesia  usually  does  not  extend  quite  to  the  median 
line  (within  one  or  two  centimetres),  but  occasionally  it 
may  extend  a  few  cm.  on  the  other  side.  It  involves 
not  only  the  skin  but  the  mucous  membranes  as  well 
(lips,  conjunctiva,  rectum,  urethra).  Hemianaesthesia 
of  organic  origin  is  always  due  to  interruption  of  the 
sensory  tract  between  the  junction  of  the  ascending 
and  descending  roots  of  the  fifth  in  the  pons  (upper 
extremity  of  the  pons)  and  the  cortex  of  the  opposite 
side  or  to  disease  of  the  cortex  itself.  Its  exact 
position  must  be  determined  by  other  symptoms. 
If  the  disease  is  in  the  pons,  the  region  supplied 
by  the  fifth  nerve  (face)  escapes  (because  the  path 
from  the  fifth  crosses  to  the  opposite  side  high  in  the 
pons),  unless  the  lesion  be  one  involving  the  entire 
formatio  reticularis  in  the  upper  part  of  the  pons.  The 
most  common  seat  of  the  lesion  causing  hemianaesthesia 
is  the  posterior  third  of  the  hinder  limb  of  the  in- 
ternal capsule  (see  Fig,  27)  between  the  lenticular  nu- 
cleus of  the  corpus  striatum  and  the  optic  thalamus.  The 
sensory  tract  is  here  contiguous  to  the  motor  path,  but 
owing  to  the  arrangement  of  the  vascular  supply  of  the 
region  it  is  common  for  a  lesion  to  injure  the  former 
without  the  latter,  or  the  latter  without  the  former, 
though  an  extensive  lesion  may  damage  both,  and  cause 
both  motor  and  sensory  symptoms.  The*  sensory  path 
in  the  capsule  also  lies  close  to  the  path  for  the 
special  senses,  which  may  be  involved  on  the  same 
side  as  tactile  sensibility,  with  the  exception  of  vision, 
the  defect  of  which  is  hemianopsia  (see  page  163). 
Hemianaesthesia  may  occur  from  disease  of  the  cortex 
itself,  or  of  the  subjacent  white  substance,  but  com- 
plete hemianaesthesia  from  this  cause  is  very  rare.  This 
is  because  the  fibres  of  the  sensory  tract  are  here  greatly 
spread  out,  to  cover  a  large  area,  and  only  a  very  ex- 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      I45 


tensive  lesion  can   involve    them    all.     Hemiansesthesia 
is  not  infrequently  of  hysterical   origin,  and   it  may  be 

one  manifestation  of  cer- 
tain traumatic  neuroses. 
In  both  these  cases  it  is 
probably  of  cortical  origin 
(nutritional  disease).  The 
points  of  distinction  be- 
tween functional  and 
organic  disease  are  con- 
sidered in  chapter  VI. 

A  partial  form  of  hemi- 
ansesthesia which  is  of  con- 
siderable importance  from 
its  frequent  occurrence  is 
that  which  accompanies 
ordinary  hemiplegia.  The 
loss  of  sensibility  does  not 
extend  to  the  median  line. 
It  exists  chiefly  or  exclu- 
sively in  the  limbs,  the  loss 
being  most  distinct  in  the 
hands  and  feet.  The  sen- 
sibility to  pain  is  usually 
diminished  in  these  cases, 
but  not  in  the  same  degree 
as  the  loss  of  tactile  sen- 
sibility. 

Crossed  HemiancBsthesia 
— (alternate  hemianses- 
thesia).— Loss  of  tactile 
sensibility  of  one  side  of  the  face  and  of  the  opposite 
limbs  is  of  rare  occurrence.  The  sensory  loss  in  the 
face  is  due  to  damage  of  the  ascending  root  of  the  fifth 


FIG.   66. 

Diagram  illustrating  the  distribution  of 
the  sensory  line  in  a  case  of  crossed  hemi- 
anaesthesia.  The  horizontal  lines  show 
the  distribution  of  the  analgesia,  which 
was  complete  above,  partial  below.  The 
vertical  lines  show  the  area  of  hyper- 
algesia. In  this  area,  contact  with  cotton 
caused  a  peculiar  prickly  sensation. 


146 


DISEASES   OF  THE   NERVOUS   SYSTEM. 


nerve  of  the  same  side  in 
the  loss  on  the  trunk  and 
sensory  tract  from 
these  parts  of  the 
opposite  side.  In  the 
pons  (below  the  up- 
per third),  and  in  the 
medulla,  these  tracts 
lie  close  together, 
hence  a  lesion  in  the 
pons  or  upper  part  of 
the  medulla  involv- 
ing the  entire  lateral 
extent  of  the  formatio 
reticularis     and    the 


some   part  of    its    course  ; 
limbs    to    damage    of   the 


Crw* 


li."S^W«rvt 


FIG.  67. 


fifth  nerve-root  gives 
rise  to  crossed  hemi- 
anaesthesia.  (See 
Fig.  67).  Crossed 
hemianaesthesia  is 
never  of  functional 
origin. 

Bilateral  A  nasi  he - 
sia,  involving  the 
limbs  on  both  sides, 
may  occur  as  a  con- 
sequence   of  disease 

of  the  pons  damaging  the  sensory  tract  on  both  sides. 
The  anaesthesia  is  seldom  complete. 

Para-AncBsihesia. — Anaesthesia  involving  both  extrem- 
ities ("  anaesthesia  of  paraplegic  distribution  "  it  is  some- 
times called)  is  generally  dependent  upon  disease  of 
the  spinal  cord  (but  not  infrequently  on  peripheral 
neuritis),  sometimes  upon  disease  of  the  cauda  equina, 


Diagram  illustrating  the  mechanism  of  crossed 
anaesthesia.  (After  Starr.)  Any  lesion  inter- 
rupting the  general  sensory  tract  from  the  lines 
above  the  crossing  of  this  tract  in  the  medulla 
and  the  ascending  root  of  the  fifth  nerve  on  the 
same  side  will  produce  crossed  anaesthesia.  The 
conditions  wiil  vary,  however,  with  the  level  of 
the  lesion.  Thus,  a  lesion  at  A  will  cause  typical 
crossed  anaesthesia  and  rotation  of  the  body  to  the 
side  of  the  lesion  from  involvement  of  the  middle 
peduncle  of  the  cerebellum  ;  a  lesion  at  1?  will 
cause  complete  anaesthesia  of  the  opposite  limbs 
and  trunk,  but  the  anaesthesia  of  the  face  on  the 
same  side  as  the  lesion  will  not  involve  the  entire 
face,  sensation  remaining  normal  in  its  upper 
portion  ;  a  lesion  at  C  will  cause  anaesthesia  of 
entire  opposite  half  of  the  body,  but  probably 
only  partial  and  greatly  limited  anaesthesia  of  the 
face  on  the  same  side  as  the  lesion. 


SYMPTOMATOLOGY    OF   NERVOUS    DISEASES.      14/ 

though  in  this  case  the  anaesthesia  usually  involves  the 
skin  on  the  lower  extremities  irregularly.  Anaesthesia 
of  the  lower  extremities  may  be  due  to  a  transverse 
lesion  (myelitis,  tumor)  or  to  a  systematic  lesion 
involving  only  the  sensory  tract  of  the  cord,  the 
posterior  median  columns.  The  upper  level  of  the 
anaesthesia  affords  an  important  indication  of  the 
upper  level  of  the  lesion,  a  more  accurate  one  than  the 
motor  palsy,  which  generally  coexists,  but  whose  exact 
distribution  and  degree  it  is  often  difficult  to  determine. 
The  exact  upper  limit  of  the  anaesthesia  in  lesions  of 
different  levels  in  the  cord  is  given  on  page  438. 

Anaesthesia  may  be  limited  to  one  extremity,  and  such 
localized  anaesthesia  may  be  of  cerebral,  spinal,  or  peri- 
pheral origin.  When  due  to  organic  disease  of  the  brain 
(hemiplegia),  as  it  occasionally  is,  the  anaesthesia  is  most 
marked  at  the  extremity  of  the  limb,  and  grows  gradually 
less  marked  as  the  trunk  is  reached — that  is,  it  has  the 
characters  of  the  common  form  of  anaesthesia  that  is 
met  in  hemiplegia  of  the  severe  or  grave  type.  If  the 
anaesthesia  corresponds  closely  to  the  area  supplied  by 
one  or  more  nerve-trunks  and  there  is  no  cincture  pain, 
it  is  probable  that  the  lesion  is  in  one  or  more  nerve- 
trunks,  or  the  plexus  above  them.  When  there  is  evi- 
dence of  a  segmental  loss  of  sensibility  (inner  border  of 
arm,  forearm,  arid  hand,  for  example)  and  there  is  a 
girdle-pain  or  sensation,  the  lesion  may  be  referred  to  a 
corresponding  segment  or  nerve-root  of  the  spinal  cord 
(especially  the  arm).  It  is  very  important  to  know  that 
anaesthesia  of  one  extremity,  with  a  sharply  limited  upper 
border  and  of  the  severe  or  grave  type,  is  frequently 
of  hysterical  origin. 

Anaesthesia  limited  to  well  defined  areas  of  the  extrem- 
ities or  trunk,  and  which  corresponds  to  the  distribution  of 


148         DISEASES   OF   THE   NERVOUS    SYSTEM. 

one  or  more  nerves  or  nerve  branches,  generally  indicates 
disease  of  the  nerve  itself, — more  rarely  disease  of  the 
nerve-roots.  In  studying  the  distribution  of  the  sensory 
loss  from  lesions  of  mixed  nerves,  it  is  helpful  to  bear 
in  mind  Schroeder  van  der  Kolk's  law,  that  the  sensory 
fibres  of  a  mixed  nerve  supply,  generally  speaking,  the 
integument  over  the  muscles  innervated  by  the  motor 
fibres  of  the  same  nerve. 

Irregular  areas  of  anaesthesia,  of  indeterminate  nerve 
supply,  are  not  infrequently  met  with  in  the  trunk  or 
limbs.  Such  patches  may  be  due  to  disease  of  the  sen- 
sory nerve-endings  in  the  skin,  to  the  irregular  incidence 
of  disease  in  the  peripheral  nerves,  to  disease  of  the 
nerve-roots,  to  systematic  disease  of  the  cord  (posterior 
sclerosis),  or  to  the  occurrence  of  irregular  islets  of 
sclerosis  in  the  cord  (multiple  sclerosis),  and  pos- 
sibly also  in  the  brain.  Perhaps  the  most  frequent 
structural  cause  of  anaesthetic  patches  is  disease  in- 
volving several  nerve-roots,  as  spinal  meningitis. 
Usually  the  localization  of  the  process  causing  the 
anaesthesia  is  easily  accomplished  with  the  help  of 
other  symptoms.  It  is  to  be  remembered  that  irregular 
areas  of  anaesthesia  are  not  infrequently  met  with  in 
hysteria,  and  are  sometimes  seen  in  neurasthenia  and 
alcoholism. 

Very  rarely  cases  are  observed  in  which  there  is 
general  loss  of  tactile  and  pain  sense,  associated  with 
tremor,  increased  reflexes  and  mental  depression, 
and  in  which  the  autopsy  gives  no  explanation  of  the 
phenomena. 

Analgesia. — Loss  of  sensibility  to  pain  may  occur  with 
or  without  loss  of  tactile  sensibility.  In  the  spinal 
cord  and  medulla  we  know  the  paths  for  these  two 
forms    of  sensibility    to  be    distinct,   and    this    explair.s 


SYMPTOMATOLOGY    OF   NERVOUS   DISEASES.      149 

the  frequency  with  which  one  form  of  sensibility  suffers 
without,  or  in  less  degree  than,  the  other,  from  disease  in 
these  situations.  In  the  brain  we  know  little  as  regards 
these  paths.  They  probably  lie  close  together,  and  both 
forms  of  sensibility  usually  suffer  together,  though  one, 
usually  tactile  sense,  is  generally  more  affected  than  the 
other.  In  disease  of  the  peripheral  nerves  and  nerve- 
roots,  also,  both  forms  generally  suffer,  though  not 
necessarily  in  equal  degree.  Where  the  two  paths  lie 
adjacent,  as  in  the  nerves  and  nerve-roots,  a  slight  grade 
of  damage  frequently  arrests  the  conduction  of  tactile 
sensation,  while  painful  impressions  continue  to  be 
transmitted.  This  probably  depends  on  the  greater 
molecular  disturbance  created  in  the  nerve  path  by 
painful  stimuli. 

What  was  said  of  the  varieties  of  anaesthesia  in  their 
bearing  on  the  position  of  the  lesion  applies  in  general 
to  analgesia.  As  regards  the  spinal  cord  the  indications 
of  the  level  of  the  lesion  are  the  same  in  disturbances 
of  tactile  and  pain  sense,  though  the  indications  as  to 
the  horizontal  position  of  the  lesion  are  different.  Anal- 
gesia may  be  of  functional  origin.  In  this  connection 
may  be  mentioned  the  delay  in  the  transmission  of  sen- 
sory impulses  (as  pain),  which  is  seen  in  some  forms  of 
spinal-cord  disease  (notably  in  tabes,  and  in  compres- 
sion of  the  cord).  The  delay  may  amount  to  five,  ten, 
twenty,  or  even  sixty  seconds.  When  marked,  such 
delay  is  evidence  of  organic  disease  (usually  of  the 
cord).  It  must  be  carefully  distinguished  from  the 
apparent  delay  which  is  seen  in  psychic  conditions 
(dementia,  delusional  states). 

Loss  of  Temperature  Sense  is  generally  observed  to  be 
associated  with  loss  of  sensibility  to  pain,  but  fre- 
quently both  forms  of  sensibility  do  not  suffer  in  equal 


150         DISEASES   OF   THE   NERVOUS   SYSTEM. 

degree,  and  one  may  be  involved  without  the  other. 
The  character  of  the  loss  varies  in  different  instances. 
Sometimes  there  is  absolute  inability  to  recognize 
either  heat  or  cold.  In  other  cases  considerable 
degrees  of  heat  and  cold  are  recognized,  while  slighter 
degrees  are  not  perceived.  The  sensibility  to  heat  and 
to  cold  is  not  always  affected  in  the  same  degree  (this 
being  due  in  all  probability  to  the  fact  that  the  conduc- 
tion of  heat  and  cold  are  subserved  by  different  nerve- 
fibres).  As  regards  the  topographical  distribution  of 
loss  of  sensibility  to  pain  in  disease,  the  same  may 
be  said,  in  general,  that  was  stated  in  regard  to  anaes- 
thesia. 

In  the  brain,  nerve-roots,  and  peripheral  nerves — that 
is,  wherever  the  sensory  paths  for  touch,  pain,  and  tem- 
perature lie  close  together,  all  three  forms  of  sensibility 
are  apt  to  suffer  together  in  disease,  and  have  the  same 
general  distribution.  But  in  the  spinal  cord  and  me- 
dulla the  tracts  for  touch  are  separated  from  those  for 
pain  and  temperature  (which  probably  lie  close  together) 
by  such  an  interval  (p.  ^^j^),  that  the  former  is  readily 
affected  without  the  latter,  and  vice  versa.  Some  ob- 
servers place  the  paths  for  pain  and  temperature  in  the 
antero-lateral  ascending  tracts  of  the  cord.  Others  be- 
lieve that  the  central  gray  matter  of  the  cord  is  concerned, 
at  least  in  part,  with  the  upward  transmission  of  these 
forms  of  sensibility.  In  the  peculiar  condition  of  the 
cord,  known  as  syringomyelia,  there  is  observed  loss  of 
pain  and  temperature  sense,  of  one  extremity  or  of  one 
side  of  the  body,  with  little  or  no  disturbance  of  tactile 
sensibility.  Focal  processes  and  injury  of  the  cord  may 
produce  the  same  effect. 

Loss  of  Muscular  Sensibility  is  observed  when  the 
path  which  conducts  impressions  from  the  muscles  be- 


SYMPTOMATOLOGY    OF   NERVOUS   DISEASES.      151 

comes  the  seat  of  disease.  As  already  stated  (p.  43),  this 
path,  after  reaching  the  posterior  nerve-roots,  with  other 
sensory  fibres,  probably  passes  up  the  cord  in  the  poste- 
rior median  column  and  direct  cerebellar  tract,  without 
undergoing  decussation.  After  reaching  the  post-pyra- 
midal nuclei,  the  tract  decussates  in  the  interolivary 
tract,  and  passes  by  the  fillet  to  the  level  of  the  posterior 
corpora  quadrigemina,  whence  fibres  probably  pass  to 
the  superior  parietal  lobule  of  the  cortex.  The  direct 
cerebellar  tract  goes  to  the  cerebellum.  Practically  loss 
of  muscular  sense  is  more  frequently  observed  in  disease 
affecting  the  peripheral  nerves  (multiple  neuritis)  and 
the  posterior  nerve-roots  (tabes)  than  in  disease  nearer 
the  brain.  Yet  it  is  met  with  in  marked  degree  in 
unilateral  and  transverse  lesions  of  the  cord.  In  unilat- 
eral disease  of  the  cord  the  loss  of  muscular  sense  exists 
only  on  the  side  of  the  lesion,  that  is,  on  the  side  of  the 
motor  loss,  and  opposite  the  general  sensory  loss.  The 
muscular  sense  may  also  be  lost  in  consequence  of  disease 
confined  to  the  interolivary  tract  in  the  medulla,  and  the 
sense  of  posture  of  a  limb  during  active  and  passive 
movement,  which  is  dependent  in  part  on  the  muscular 
sense  (cutaneous  and  joint  sensations  being  the  other 
factors),  may  be  much  impaired  or  lost  from  disease  of 
the  cortex,  and  probably  also  of  the  central  ganglia. 
There  is  every  reason  to  believe  that  the  sense  of  posture 
is  regularly  impaired  in  the  limbs  of  the  opposite  side 
whenever  there  is  destructive  disease  of  the  superior 
parietal  lobule. 

Hyper cBsthesia  and  Hyperalgesia. — Increased  sensibility 
to  pain  is  designated  hyperalgesia,  or,  less  correctly, 
hypersesthesia.  Probably  there  is  no  cutaneous  hyper- 
aesthesia  in  the  sense  of  increased  tactile  sensibility, 
with   recognition    of   two    points   of   the    aesthesiometer 


152         DISEASES    OF   THE    NERVOUS   SYSTEM. 

at  smaller  distances  than  normal.  Sometimes  a  light 
touch  on  the  skin  causes  pain,  or  an  unpleasant  sensation, 
but  this  is  probably  due  to  irritation  of  over  sensitive 
end-organs  which  subserve  common  sensibility  (pain), 
and  not  to  increased  tactile  acuteness.  This  increased 
sensitiveness  is  frequently  due  to  irritation  of  sensory 
fibres  in  some  part  of  their  course — peripheral,  spinal,  or 
cerebral.  Probably  the  irritation  is  operative  by  exalting 
the  sensory  impression  as  it  passes,  but  it  may  also  act 
by  increasing  the  irritability  of  the  cortical  sensory 
centres.  The  distribution  of  the  sensory  disturbance  is 
sometimes  of  service  in  localizing  the  position  of  the 
lesion,  and  the  same  general  statements  are  applicable 
that  have  been  mentioned  in  connection  with  anaes- 
thesia. Increased  cutaneous  sensibility  is  observed  in  a 
variety  of  processes — as  meningitis,  cerebral  and  spinal 
tetanus,  hydrophobia,  hysteria,  traumatic  neuroses,  etc. 
It  is  a  common  and  important  symptom  of  neuritis  and 
multiple  neuritis.  When  tactile  or  painful  stimuli  give 
rise  to  perverted  forms  of  sensation,  as  numbness,  tin- 
gling, or  formication,  these  are  designated  paraesthesiae. 
Paraesthesiae  may  have  a  purely  subjective  origin,  or  they 
may  be  of  cerebral,  spinal,  or  peripheral  origin. 

Pai7i^  another  expression  of  sensory  irritation,  is  an 
important  symptom  of  organic  disease  of  the  nervous 
system.  It  is,  however,  so  common  in  functional  affec- 
tions, that  many  varieties  of  pain  are  in  themselves  of 
little  diagnostic  importance.  Severe  recurrent  limb 
pains  may  arise  from  any  form  of  nervous  disease  which 
involves  the  sensory  tract  and  partially,  but  only  par- 
tially, destroys  it.  As  examples,  may  be  mentioned  the 
pains  of  multiple  neuritis  from  neural  irritation,  of 
spinal  meningitis,  spinal  tumor,  spinal  compression,  and 
locomotor  ataxia,  from  irritation  of  the  posterior  nerve- 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      1 53 

roots,  of  myelitis  from  irritation  of  sensory  structures 
within  the  cord,  of  cerebral  .hemorrhage,  softening,  or 
tumor  involving  the  sensory  tract  in  the  internal  capsule, 
and  of  irritative  processes  in  the  motor  cortex.  Pain  in 
the  distribution  of  the  fifth  nerve  is  an  important  and 
early  symptom  of  disease  of  the  nucleus  or  trunk  of  the 
nerve.  The  pains  that  result  from  irritation  of  the  nerve- 
roots  by  vertebral  disease  are  generally  increased  by 
movement.  This  is  often  marked  in  vertebral  cancer 
and  caries. 

Pain  Referred  to  the  Spinal  Column  is  not  infrequently 
observed  in  disease  involving  the  vertebrae  and  the  dura 
mater.  Occasionally  it  is  met  with  in  spinal-cord  disease 
of  long  standing,  as  myelitis.  It  is  then  often  referred  to 
the  parts  in  the  vicinity  of  the  spine,  as  the  sacrum  and 
loins,  as  well  as  to  the  spine  itself.  Its  mechanism  and 
exact  significance  are  not  known.  Where  there  is 
organic  disease  of  the  bones,  pain,  often  severe,  is  a 
persistent  symptom,  and  is  usually  associated  with  local 
tenderness,  but  the  same  association  of  spontaneous  pain 
and  tenderness  to  pressure  is  seen  in  the  purely  neuralgic 
affection  of  the  spine  known  as  *'  rachialgia." 

Sometimes  the  pains  of  chronic  spinal-cord  disease, 
and  of  acute  processes,  are  not  acute,  but  dull  and  per- 
sistent. These  pains  are  often  regarded  as  rheumatic, 
particularly  when  exacerbations  occur,  as  they  frequently 
do  in  chronic  disease,  during  wet  or  cold  weather.  Per- 
sistent or  rheumatoid  pains  in  the  limbs  should  always 
lead  to  a  search  for  more  unequivocal  evidences  of 
spinal-cord  disease — such  as  slight  localized  loss  of 
power,  anaesthesia,  or  altered  reflex  action. 

Cincture  Pain  (girdle-pain)  is  a  persistent  sense  of 
painful  constriction,  as  of  a  band  encircling  the  body, 
the  limbs,  or  the  neck.     It  is  most  frequently  observed 


154         DISEASES   OF   THE   NERVOUS   SYSTEM. 

in  cases  where  the  cord  is  damaged  transversely,  as  in 
myelitis,  and  fracture  or  dislocation  of  the  vertebrai. 
The  pain  is  due  to  the  irritation  of  sensory  structures 
just  above  the  seat  of  the  lesion — that  is,  in  the  lowest 
part  of  the  healthy  cord,  and  is  referred,  as  is  the  rule, 
to  the  peripheral  sensory  nerve-endings.  It  possesses 
considerable  diagnostic  significance,  for  it  is  not  only 
evidence  of  organic  disease,  but  indicates  the  upper 
level  of  the  lesion  in  the  cord.  A  cincture  pain  also 
occurs  in  locomotor  ataxia,  but  is  far  less  frequently 
observed  than  in  myelitis. 

Muscular  Tenderness  (muscle  pain  sense)  is  a  symp- 
tom which,  from  its  constancy  in  some  diseases  of 
the  peripheral  nerves  (multiple  neuritis)  and  muscles 
(polymyositis),  is  of  diagnostic  importance.  In  poly- 
myositis the  muscles  are  exceedingly  painful  on  pres- 
sure, though  there  may  be  little  spontaneous  pain, 
except  on  movement.  In  multiple  neuritis  there  are  neu- 
ritic  pains  and  tenderness  of  the  nerve-trunks,  but  the 
sensitiveness  of  the  muscles  to  pressure  is  even  more 
constant.  The  occurrence  of  muscular  tenderness  in 
trichiniasis  must  be  remembered  in  this  connection.  It 
is  usually  associated  with  considerable  spontaneous  pain. 

Headache. — The  head  is  very  frequently  the  seat  of 
pain.  In  a  large  majority  of  cases  this  pain  is  the  ex- 
pression of  functional  derangement,  which  is  of  widely 
different  character  in  different  cases.  The  headaches 
which  result  from  gastric  disturbance,  anaemia,  febrile 
conditions,  renal  disease,  various  forms  of  toxaemia  and 
errors  of  refraction,  probably  constitute  more  than 
ninety-five  per  cent,  of  all  the  headaches  met  with  in 
general  practice.  But  organic  disease  within  the  cranial 
cavity  is  also  a  frequent  cause  of  headache,  and  the 
importance    of    distinguishing   between    functional    dis- 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      155 

turbance  and  organic  intracranial  processes  makes  it 
necessary  to  study  carefully  the  character  of  every  case 
of  headache. 

The  pain  of  organic  disease  is  usually  constant.  It 
varies  in  degree  from  time  to  time>  but  the  patient  is 
seldom  entirely  free  from  it.  The  severity  of  the  pain  is 
also  a  suggestive  feature.  In  a  considerable  proportion 
of  cases  the  pain  is  at  times  intensely  severe.  It  persists 
through  the  night,  and  either  prevents  the  patient  from 
sleeping  or  awakens  him  from  his  sleep.  This  is  an  im- 
portant diagnostic  point,  for  the  headache  of  functional 
disease  rarely  prevents  sleep.  Whenever,  therefore,  a 
patient  complains  that  his  headache  frequently  keeps 
him  awake  during  the  night,  the  possibility  of  organic 
brain  disease  should  be  thought  of,  and  other  evidences 
of  such  disease  should  be  sought.  But  it  must  not  be 
forgotten  that  in  point  of  severity  alone  some  functional 
headaches,  as  neuralgia  and  migraine,  resemble  closely 
the  pain  of  organic  diseases.  Their  paroxysmal  char- 
acter and  short  duration  make  an  error  in  diagnosis 
impossible. 

The  pain  of  organic  disease  is  increased  by  anything  that 
leads  to  increased  vascular  tension  within  the  cranium,  as 
stooping  or  coughing,  but  this  is  not  a  distinctive  feature 
of  such  disease.  The  headache  of  organic  disease  is  some- 
times diffuse,  sometimes  frontal  or  occipital,  or  both  ; 
sometimes  it  is  distinctly  one-sided,  and  occasionally  it  is 
sharply  localized.  Pain  which  is  very  limited  in  extent 
is  more  apt  to  be  functional  than  organic  in  origin.  Pain 
that  is  one-sided  is  seldom  due  to  disease  of  an  opposite 
region  of  the  brain,  but  it  is  never  possible  to  say,  from 
the  headache  alone,  whether  there  is  a  close  correspond- 
ence between  the  seat  of  pain  and  the  seat  of  the  lesion. 
If  the  disease  is  at  the  surface  of  the  brain,  or  in  the 


156         DISEASES   OF   THE   NERVOUS   SYSTEM. 

meninges,  or  very  near  the  surface,  there  is  probably  a 
close  correspondence  between  the  two.  When  the  dis- 
ease is  thus  superficial  there  is  often  local  tenderness  on 
light  percussion  over  the  seat  of  the  lesion.  Sometimes 
no  correspondence  exists  between  the  seat  of  the  head- 
ache and  the  lesion — for  example,  the  headache  is  some- 
times frontal  when  the  lesion  is  in  the  cerebellum. 

The  intracranial  processes  which  give  rise  to  head- 
ache are  generally  irritative  and  progressive  in  character, 
as,  for  example,  tumor,  abscess,  and  the  different  varie- 
ties of  meningitis.  Nevertheless,  little  or  nothing  is 
known  as  to  the  mechanism  by  which  these  processes 
give  rise  to  pain  ;  even  the  structures  which  are  the  seat 
of  pain  cannot  be  positively  designated.  The  dura  mater 
receives  sensory  nerve  filaments  and  may  unquestiona- 
bly be  the  seat  of  pain  when  the  membrane  is  the  seat  of 
disease,  and  probably  also  when  it  is  not  the  seat  of 
appreciable  structural  change.  The  brain  of  a  highly 
organized  animal  may  be  mutilated  without  giving  rise 
to  evidences  of  pain,  but  neither  this  fact  nor  the  cir- 
cumstance that  sensory  fibres  have  not  yet  been  dis- 
covered in  the  pia-mater  or  the  cerebral  substance  can 
be  regarded  as  showing  that  those  structures  are  insensi- 
ble to  pain  under  conditions  of  disease.  It  has  been 
supposed  that  increased  intracranial  pressure  is  operative 
in  the  production  of  headache  in  certain  diseases,  but 
while  this  may  be  a  factor  in  some  cases,  it  has  been 
shown  that  processes  which,  like  internal  hydrocephalus, 
increase  the  intracranial  pressure  as  much  as  it  is  ever 
increased,  but  cause  no  tissue  irritation,  often  run  their 
course  without  causing  headache. 

We  have  seen  that  the  constancy  and  severity  of  a 
headache  may  be  suggestive,  perhaps  highly  suggestive, 
of  intracranial   disease.     Yet   these   characteristics  of  a 


SYMPTOMATOLOGY   OF   NERVOUS    DISEASES.      157 

headache  never  prove  the  existence  of  organic  disease. 
Actual  proof  can  be  supplied  only  by  the  association 
with  headache  of  other  evidences  of  disease.  Of  these 
optic  neuritis  is  the  most  significant.  But  double  optic 
neuritis  and  headache  occur  as  symptoms  of  certain  con- 
stitutional states,  notably  lead  poisoning,  chronic  diffuse 
nephritis,  and  a  high  grade  of  anaemia.  If  we  can  ex- 
clude these  conditions,  we  may  regard  the  occurrence  of 
marked  double  optic  neuritis  with  headache  as  evidence 
of  some  form  of  organic  intracranial  disease. 

It  is  hardly  necessary  to  say  that  neither  the  absence 
of  headache  nor  its  slight  character  in  any  particular 
case  renders  it  possible  to  exclude  organic  disease.  In 
the  presence  of  symptoms  of  doubtful  character,  the 
absence  of  headache  is  of  some  significance  in  lessening 
the  probability  of  the  existence  of  organic  disease,  but 
in  the  presence  of  unequivocal  symptoms,  such  as  local 
paralysis  or  convulsions,  its  absence  does  not  materially 
modify  the  diagnosis. 

Cephalic  Sensations  Other  than  Pain  are  frequently 
complained  of  by  patients  who  are  hypochondriacal 
or  neurasthenic,  or  whose  brains  are  overworked.  The 
sensations  are  variously  described.  Very  frequently 
there  is  a  sense  of  pressure,  slight  or  great,  as  if  the  top 
of  the  skull  were  being  forced  in.  Sometimes  the  pa- 
tient feels  as  if  the  sides  of  the  head  were  being  forced  in, 
but  generally  the  sensation  is  referred  to  the  vertex.  A 
feeling  of  expansion,  as  if  the  top  of  the  skull  were 
being  lifted,  is  often  complained  of.  Another  and  more 
common  sensation,  described  chiefly  by  neurasthenics, 
is  a  crackling  feeling  within  the  skull  as  if  something 
had  broken,  followed  often  by  a  curious  sense  of  empti- 
ness or  lightness  of  the  head.  Sometimes  there  is  sim- 
ply a  sense  of  fulness  of  the  head  or  a  sense  of  throb- 


158         DISEASES   OF   THE   NERVOUS   SYSTEM. 

bing.  These  sensations  and  many  more  are  very  often 
described  in  extravagant  language.  They  are  seldom 
constant,  and  are  always  functional.  They  are  generally 
aggravated  by  attention.  We  are  in  ignorance  as  to  how 
these  sensations  are  produced,  but  there  is  no  reason 
for  attributing  them  to  cerebral  congestion,  or  to  con- 
gestion at  the  base  of  the  brain. 

Symptoms  Referable  to  the  Special  Senses. 

Olfactory  Symptoms. — Anosmia,  loss  of  smell,  is 
much  more  frequently  the  result  of  disease  of  the  olfac- 
tory mucous  membrane  (chronic  inflammation,  polypi), 
than  of  intracranial  disease,  and  such  local  disease  must 
be  excluded  before  the  symptom  can  be  considered  sig- 
nificant of  brain  disease.  Blows  on  the  head  have  been 
known  to  cause  anosmia  by  mechanically  tearing  the 
olfactory  filaments  from  the  bulb,  but  this  is  an  infre- 
quent occurrence.  Another  rather  infrequent  cause  of 
anosmia  is  pressure  on  the  nerve  or  bulb  by  tumor  in 
the  anterior  fossa  of  the  skull,  or  by  bone  disease. 
Meningitis  may  also  involve  the  nerve,  and  it  has  been 
compressed  in  internal  hydrocephalus.  Rarely  anosmia 
occurs  in  degenerative  diseases  of  the  nervous  system, 
as  locomotor  ataxia,  and  dementia  paralytica.  Disease 
in  the  sensory  part  of  the  internal  capsule  (posterior 
limb)  has  caused  anosmia  on  the  side  opposite  the  lesion. 
An  extensive  cortical  or  subcortical  lesion  occasionally 
produces  the  same  effect.  Disease  of  the  tip  of  the 
temporo-sphenoidal  lobe,  involving  the  olfactory  centre, 
may  unquestionably  give  rise  to  anosmia  on  the  same 
side  as  the  lesion.  Functional  loss  of  smell  may  occur 
in  hysteria.  It  is  always  associated  with  other  forms  of 
sensory  loss,  hemianaesthesia,  crossed  amblyopia,  loss 
of  taste,  etc.     In   attaching  significance  to  the  presence 


SYMPTOMATOLOGY    OF   NERVOUS   DISEASES.      1 59 

of  anosmia,  it  must  be  remembered  that  it  is  sometimes 
congenital  (due  to  congenital  absence  of  the  bulbs),  and 
that  it  may  result  indirectly  from  disease  of  the  trigem- 
inus, through  trophic  changes  in  the  olfactory  mucous 
membrane,  or  from  defective  local  secretion. 

Hyperosmia  or  Olfactory  Hyperesthesia  is  occasionally 
observed  in  hysteria.  It  consists  in  the  development  of 
great  acuteness  in  the  sense  of  smell,  so  that  odors  are 
perceived  which  are  ordinarily  not  recognized.  The 
symptom  has  little  diagnostic  significance. 

Olfactory  Hallucinations. — Subjective  sensations  of 
smell  may  be  of  functional  or  organic  origin.  In  in- 
sanity they  are  not  very  uncommon.  The  epileptic  par- 
oxysm is  sometimes  ushered  in  with  an  olfactory  aura, 
usually  unpleasant  in  character.  In  several  instances 
the  development  of  gross  organic  disease  (tumor)  of  the 
anterior  part  of  the  temporo-sphenoidal  lobe  has  been 
accompanied  by  olfactory  aurse.  An  aura  may  also  result 
from  disease  involving  the  olfactory  tract.  The  repeated 
occurrence  of  such  an  aura  is  of  great  diagnostic  signifi- 
cance in  the  presence  of  evidence  of  organic  disease, 
for  it  gives  a  clue  to  the  position  of  the  lesion,  sometimes 
when  other  indications  are  wanting. 

Visual  Symptoms. — Amblyopia  and  Amaurosis  are 
terms  used  to  designate  different  degrees  of  visual  defect, 
theformer  meaning  a  partial  loss  or  blurring  of  sight,  the 
latter  complete  blindness.  Complete  blindness  (of  nervous 
origin)  of  one  eye,  indicates  that  the  optic  nerve  is  dam- 
aged between  that  eye  and  the  chiasma — that  is,  in  the 
orbit,  at  the  optic  foramen,  or  within  the  skull  between  the 
foramen  and  the  chiasm.  Such  damage  may  result  from 
pressure  by  tumors,  from  basal  disease,  from  inflammation, 
and  from  embolism  of  the  central  artery  of  the  retina,  etc., 
but  in  these  cases  the  blindness  is  not  always  absolute. 


l6o        DISEASES   OF  THE   NERVOUS   SYSTEM. 

Frequently  there  is  concentric  limitation  of  the  field, 
and  sometimes  there  are  regular  defects.  Amblyopia  of 
one  eye  may  also  result  from  disease  of  considerable 
extent  in  the  cortex  of  the  opposite  hemisphere,  involv- 
tng  the  lower  and  posterior  part  of  the  parietal  lobe 
(angular  and  supra-marginal  convolutions).  There  is 
usually  considerable  limitation  of  the  visual  field  in  such 
cases,  and  though  the  patient  does  not  notice  any  defect 
in  the  vision  of  the  other  eye,  examination  usually  reveals 
a  slight  concentric  restriction  of  the  field  of  that  side. 
Hemiansesthesia  is  also  frequently  observed  in  these 
cases,  and  its  occurrence  helps  in  the  distinction  of  crossed 
amblyopia  from  the  amblyopia  of  optic-nerve  disease. 
Other  points  of  distinction  are  as  follows  :  (i.)  the 
pupillary  reaction  is  diminished  in  disease  of  the  optic 
nerve,  but  is  normal  in  cortical  disease  ;  (2.)  The  motor 
nerves  of  the  eyeball  are  frequently  involved  in  optic- 
nerve  disease,  never  in  disease  of  the  parietal  cortex. 
Functional  loss  of  vision  of  one  eye  only  is  exceedingly 
rare,  but  may  result  in  a  reflex  manner  from  irritation  of 
the  fifth  nerve,  and,  rarely,  from  hysteria.  In  hysterical 
amblyopia,  which  is  almost  always  unilateral,  vision  may 
amount  to  complete  blindness.  The  fields  are  contracted 
concentrically,  and  since  the  retina  exhausts  rapidly,  the 
limitation  may  be  more  marked  with  each  succeeding 
test  at  the  one  examination.  A  functional  -  amblyopia 
affecting  both  eyes,  as  in  organic  crossed  amblyopia,  and 
associated  with  hemianaesthesia,  is  sometimes  observed  in 
hysteria.  This  functional  form  is  much  more  frequent 
than  the  organic  form,  though  it  is  probably  not  as 
common  as  has  been  supposed. 

Bilateral  loss  of  vision,  partial  or  complete,  is  infre- 
quently observed  in  the  course  of  organic  disease  of  the 
nervous  system,  as  the  result  of  optic  neuritis  or  optic 
atrophy,  primary  or  post-neuritic.     The  relation  of  these 


SYMPTOMATOLOGY   OF  NERVOUS   DISEASES.       l6l 

processes  to  intracranial  disease  will  be  discussed  else- 
where. It  is  important  to  bear  in  mind  the  fact  that  a 
considerable  error  in  refraction  often  gives  rise  to  ambly- 
opia, and  that  such  an  affection  must  be  excluded  before 
we  can  attribute  the  visual  defect  to  disease  of  the  optic 
nerve. 

Defective  Central  Vision  sometim'es  results  from  ir- 
regular patches  (scotomata)  of  retinal  anaesthesia  in- 
volving the  fixing  point  (macula  lutea),  and  extending 
a  very  little  distance  about  it.  Such  central  scotomata 
tend  to  be  symmetrical  in  situation,  though  the  vision  of 
one  eye  may  be  more  impaired  than  that  of  the  other. 
The  visual  loss  is  seldom  absolute,  even  in  the  portion 
of  the  field  where  it  is  most  decided,  and  the  loss  for 
colors  is  usually  more  extensive  than  that  for  white 
light.  This  form  of  amblyopia  is  met  with  in  those  who 
use  tobacco  to  excess  ("  tobacco  amblyopia"),  and  occa- 
sionally occurs  from  the  excessive  use  of  alcohol.  It  is 
generally  a  transient  affection,  and  for  this  reason  is 
often  classed  with  functional  amblyopia,  but  it  is  really 
due  to  an  inflammation  of  the  central  fibres  of  the  optic 
nerve  (axial  neuritis). 

Temporary  amblyopia,  involving  both  eyes,  occurs  in 
certain  functional  diseases  of  the  brain,  notably  epilepsy 
and  migraine,  but  there  is  little  danger  of  confounding 
this  with  amblyopia  of  organic  origin,  as  the  loss  of 
vision  is  not  only  transient  but  distinctly  paroxysmal  in 
character.  In  epilepsy  the  loss  of  sight  usually  just 
precedes  loss  of  consciousness.  In  migraine  the  defect 
of  vision  is  always  partial,  and  may  consist  in  general 
blurring  of  sight,  or  in  unilateral  defect  in  each  eye — 
hemianopsia. 

Functional  amblyopia  of  one  eye  from  irritation  of 
the  fifth  nerve  has  been  alluded  to.  But  such  reflex  am- 
blyopia is  more  often    bilateral  than  one-sided,  though 


l62  DISEASES   OF   THE   NERVOUS   SYSTEM. 

the  loss  of  sight  is  frequently  most  marked  on  the  side 
of  the  nerve  which  is  the  seat  of  irritation.  The  pain 
of  neuralgia  may  be  effective  in  producing  reflex  ambly- 
opia ;  sometimes  the  cause  is  the  irritation  of  a  carious 
tooth,  generally  a  molar.  How  such  causes  are  effective  is 
not  definitely  known.  Probably  the  arrest  of  visual  func- 
tion is  the  result  of  inhibition  exerted  on  the  nervous  ele- 
ments of  the  retina,  or  on  the  visual  centres  of  the  cortex. 

Bilateral  loss  of  sight,  usually  of  short  duration,  but 
often  complete  in  degree,  is  sometimes  met  with  as  a 
consequence  of  toxic  blood-states — "toxic  amblyopia" 
it  is  called.  Uraemic  poisoning  is  the  most  frequent 
cause  of  such  blindness  (which  is  frequently  of  sudden 
onset).  It  may  also  occur  in  malaria,  which  disappears 
on  exhibiting  full  doses  of  quinine.  Oddly  enough,  a 
similar  defect  also  occurs  in  poisoning  by  quinine.  Lead 
occasionally  produces  similar  results.  There  are  usually 
no  ophthalmoscopic  changes  to  which  the  blindness  in 
these  cases  can  be  ascribed. 

Concentric  Limitation  of  the  Visual  Field,  both  for  white 
light  and  for  colors,  is  observed  in  many  of  the  affec- 
tions that  have  been  mentioned  as  causes  of  ambly- 
opia. If  we  exclude  those  cases  in  which  the  limitation 
is  the  result  of  structural  change  in  the  optic  nerve 
(neuritis,  atrophy)  there  remain  a  number  of  conditions 
of  the  nervous  system,  both  functional  and  organic,  in 
which  this  limitation  is  of  frequent  occurrence.  Of 
these  conditions  the  following  are  of  especial  importance  : 
crossed  amblyopia  of  organic  origin,  crossed  amblyopia 
of  hysterical  origin,  crossed  amblyopia  occurring  in  the 
course  of  the  traumatic  neuroses,  the  amblyopia  of  epi- 
lepsy and  of  neurasthenia,  and  the  amblyopia  of  multiple 
sclerosis.  The  acuity  of  central  vision  may  be  impaired 
in  any  of  these  conditions,  but  in  some  of  them  (e.  g.^ 
the  traumatic  neuroses)  it  is  frequently  normal. 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.       163 

Hemianopsia.^ — Hemianopsia  is  loss  of  vision  in  one 
lateral  or  vertical  half  of  the  visual  field.  It  almost 
always  involves  both  visual  fields,  but  partial  damage  to 
one  optic  nerve  occasionally  gives  rise  to  a  unilateral 
hemianopsia.  In  bilateral  hemianopsia  either  one  hori- 
zontal or  vertical  half  of  each  field  may  be  obscured. 
A  horizontal  defect  is,  however,  exceedingly  rare.  Ver- 
tical hemianopsia,  on  the  contrary,  is  not  very  infrequent, 
and  constitutes  a  symptom  of  the  greatest  importance 
for  the  localization  of  cerebral  lesions.  Several  varieties 
of  bilateral  vertical  hemianopsia  (which  is  always  due  to 
an  intracranial  lesion)  must  be  distinguished. 

A. —  Temporal  or  Bi- Temporal  Hemianopsia^  is  that 
variety  in  which  the  temporal  half  of  each  field  is 
obscured.  It  therefore  represents  a  defect  of  the  nasal 
half  of  each  retina,  which  can  result  only  from  disease 
of  the  central  portion  of  the  optic  chiasm,  involving  the 
decussating  fibres  of  each  retina.  Often  the  process 
(tumor  or  inflammation)  which  gives  rise  to  temporal 
hemianopsia  extends  laterally,  and  involves  the  non-de- 
cussating fibres  of  one  side  of  the  chiasma,  thus  causing 
total  blindness  of  the  corresponding  eye,  or,  if  both 
sides  of  the  tract  are  involved,  of  both  eyes.  In  some 
cases  of  temporal  hemianopsia  from  syphilis  at  the  base, 
a  rapid  and  frequent  variation  of  the  dark  half-fields  has 
been  noted  (so  called  "  oscillating  bi-temporal  hemian- 
opsia ").  It  is  probably  of  some  diagnostic  importance, 
as  evidence  of  basal  syphilis  (gumma,  chronic  menin- 
gitis),   but  cannot  be  regarded  as  pathognomonic. 

'  The  word  hemiopia  is  properly  used  to  designate  loss  of  sight  in 
one  half  of  the  retina.  A  left  hemiopia  is  therefore  equivalent 
to  a  right  hemianopsia,  and,  conversely,  a  right  hemiopia  to  a  left 
hemianopsia.  The  word  hemianopia  is  used  synonymously  with  hemi- 
anopsia. Lateral  hemianopsia  is  also  known  as  homonymous 
hemianopsia. 


164         DISEASES   OF   THE   NERVOUS   SYSTEM. 

B. — Nasal  Hemianopsia. — Obscuration  01  the  nasal 
half  of  each  field  from  anaesthesia  of  the  temporal  half 
of  each  retina  is  not  only  the  rarest  form  of  hemianopsia 
but  is  the  rarest  of  all  visual  defects,  since  it  can  result 
only  from  a  lesion  which  involves  each  side  of  the  optic 
chiasm  without  damaging  the  central  part.  In  one  case, 
such  hemianopsia  was  produced  by  the  pressure  of  cal- 
cified and  enlarged  carotid  arteries  on  the  sides  of  the 
chiasm. 

C. — Lateral y  or  Ho7no7iymous  Hemianopsia^  is  that 
form  of  hemianopsia  in  which  corresponding  visual 
fields  are  obscured.  Thus,  in  right  lateral  hemianopsia 
both  right  half -fields  are  blind.  In  all  cases  of  lateral 
hemianopsia  the  lesion  is  posterior  to  the  optic  chiasm. 
It  may  be  in  one  optic  tract,  in  one  of  the  primary  optic 
centres  (corpora  geniculata  externa),  in  the  pulvinar  of  the 
thalamus,  in  the  sensory  tract  of  the  internal  capsule,  in 
the  optic  radiation,  in  the  occipital  lobe,  or  in  the  half- 
field  centre  of  the  cortex  (cuneus).  In  whichever  one  of 
the  enumerated  positions  the  lesion  lies,  it  is  on  the  side 
opposite  the  half-fields  obscured.  A  lesion  of  the  an- 
gular gyrus  may  also  cause  lateral  hemianopsia,  but 
probably  it  can  do  so  only  by  injuring  the  immediately 
underlying  optic  radiation.  The  determination  of  the 
position  of  the  lesion  in  the  optic  apparatus  is  based  on 
the  associations  of  the  hemianopsia.  The  extent  of  the 
half  loss  of  the  visual  fields  varies  in  different  instances. 
The  line  of  division  between  the  obscured  and  seeing 
halves  may  pass  through  the  fixing  point  (corresponding 
to  the  macula  lutea),  or  may  pass  just  to  one  side  of  it, 
leaving  it  within  the  region  of  sight.  These  are  the 
typical  forms  of  hemianopsia.  In  other  instances  the 
line  of  division  is  irregular,  or  inclines  obliquely  to  one 
side  or  the  other  above  and  below  the  fixing  point. 
These  variations  do  not  depend  on   the  position  of  the 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.       165 

lesion  causing  the  hemianopsia,  but  on  individual  pecu- 
liarities in  the  decussation  in  the  optic  nerves.  Certain 
other  variations,  however,  are  related  to  the  situation  of 
the  lesion.  In  the  first  place,  hemianopsia  may  be  incom- 
plete, a  portion  only  of  the  half-fields  being  obscured. 
The  area  of  defective  vision  is  in  these  cases  sector-like, 
being  frequently  irregularly  quadrantic  in  outline.  This 
incomplete  loss  is  probably  dependent  on  partial  destruc- 
tion of  the  visual  path,  or  half-vision  centre,  most  fre- 
quently the  latter.  Secondly,  lateral  hemianopsia  may 
be  associated  with  concentric  limitation  of  the  half-fields 
of  vision  that  remain.  This  limitation  of  the  remaining 
fields  is  always  greatest  in  the  eye  of  the  side  opposite 
the  lesion.  It  probably  indicates  that  the  lesion  involves 
not  only  the  half-vision  centre  of  the  cortex,  or  the  optic 
fasciculus  in  the  occipital  lobe,  but  also  the  higher  visual 
apparatus  (see  page  50),  which  is  supposed  to  lie  in 
and  beneath  the  inferior  parietal  lobe.  In  about  one 
ha-lf  of  the  cases  of  hemianopsia  the  symptom  is  associ- 
ated with  transient  or  permanent  hemiplegia  of  organic 
origin,  both  symptoms  being  effects  of  the  same  lesion. 
The  hemiplegia  is  on  the  side  of  the  loss  of  vision  ;  the 
patient  "  cannot  see  his  paralyzed  side."  Complete  loss 
of  sight  in  both  eyes  occasionally  results  from  double 
lateral  hemianopsia.  It  depends  on  the  occurrence  of  two 
lesions,  one  in  each  hemisphere,  involving  the  visual  path 
posterior  to  the  chiasm. 

Lateral  hemianopsia  which  has  been  complete  for 
several  months,  seldom  passes  away  entirely.  It  may 
remain,  with  little  change,  during  many  years  ;  m  one 
case  it  is  known  to  have  endured  twenty-three  years.  It 
is  important  to  know  that  hemianopsia  may  exist  for  a 
considerable  time  without  being  noticed  by  the  patient. 

Lateral  hemianopsia  is  not  a  very  uncommon  symptom 
of  migraine.     It  is  of  short  duration,  and  often  the  loss 


l66         DISEASES   OF   THE   NERVOUS    SYSTEM. 


FIG.    68. 

Diagram  illustrating  the  course  of  the  optic  and  visual  tracts.  (AfterStarr.) 
A,  lesion  of  left  optic  nerve,  causing  total  blindness  in  left  eye  ;  B,  lesion  causing 
bilateral  temporal  hemianopsia  ;  C,  C,  lesions  in  the  optic  or  visual  path  posterior 
to  the  chiasm.  All  such  lesions  cause  bilateral  homonymous  hemianopsia,  but  give 
rise  to  different  associated  symptoms  according  to  the  position  of  the  lesion.  Thus, 
a  lesion  in  the  int.  capsule,  as  at  C,  causes  also  hemiplegia  of  the  opposite  side  of 
the  body. 
The  rest  of  the  diagram  requires  no  explanation. 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      167 

involves  the  right-half  fields  in  one  attack,  and  the  left- 
half  fields  in  another.  Not  infrequently  other  forms  of 
visual  disturbance  occur  during  other  attacks.  It  is  well 
to  bear  in  mind  the  fact  that  the  hemianopsia  of  migraine 
may  occur  as  an  isolated  symptom,  though  it  is  usually 
associated  with  some  degree  of  headache  and  gastric 
disturbance.  It  is  probable  that  migraine  is  the  chief 
functional  affection  in  which  hemianopsia  occurs.  It  is 
exceedingly  probable  that  the  symptom  is  only  rarely  of 
hysterical  origin.  Transient  hemianopsia  is  frequently 
observed  during  the  onset  of  cerebral  hemorrhage,  but 
in  this  case  it  is  probably  an  indirect  symptom,  due  to 
inhibition  of  the  cortical  centre  by  irritation.  In  almost 
all  cases  of  hemianopsia  the  loss  of  vision  for  white  light 
is  associated  with  a  corresponding  loss  for  colors.  It 
occasionally  happens,  however,  that  there  is  hemianopsia 
for  colors — "  hemi-achromatopsia,"  it  is  called — w^hen 
there  is  no  loss  whatever  for  white.  In  these  cases  an 
object,  when  moved  across  the  field,  is  seen  in  all 
positions,  but  becomes  uniformly  gray  when  moved 
beyond  the  vertical  line  of  separation  between  the  half- 
fields.  The  explanation  of  this  remarkable  phenomenon 
must  lie  in  the  existence  of  a  distinct  centre  for  color 
vision,  adjacent,  in  all  probability,  to  the  half -vision 
centre  in  the  cuneus. 

Symptoms  referable  to  irritation  of  the  optic  apparatus 
occasionally  appear  in  the  course  of  organic  processes 
which  eventually  give  rise  to  atrophy  or  inflammation 
of  the  optic  nerve,  but  such  phenomena  are  of  much 
more  frequent  occurrence  in  functional  and  nutritional 
disturbances  of  the  nervous  system.  Muscse  volitantes, 
sparks,  etc.,  not  infrequently  appear  to  pass  before  the 
eyes  of  neurasthenic  and  hysterical  patients.  A  zigzag 
appearance,  described  as  the  '^  fortification  spectrum,"  is 
often    seen    in   migraine,   but    is   not    met    with    in    any 


l68         DISEASES    OF   THE   NERVOUS   SYSTEM. 

Other  neurosis,  except  in  rare  cases  of  epilepsy.  It 
usually  lasts  many  minutes.  Sparks,  flashes  of  light, 
colors  before  the  eyes,  and  other  irritative  symptoms 
related  to  the  visual  apparatus  occur  in  migraine,  and 
also  in  epilepsy.  In  epilepsy  a  visual  aura  is  not  un- 
common ;  indeed,  such  an  aura  is  more  frequent  in 
epilepsy  than  all  other  warnings  of  the  special  senses 
combined.  Sometimes  these  impressions  are  very  elabo- 
rate, and  may  represent  a  complex  perception,  as  of 
a  human  face  ;  usually  they  consist  of  crude  sensations, 
such  as  luminous  flashes,  etc.  Rarely  a  visual  aura  is  a 
precursor  of  convulsions  due  to  organic  cerebral  disease. 
In  most  cases  of  this  kind  the  lesion  has  been  located  iji 
the  cortex  or  white  substance  of  the  occipital  lobe. 

Ophthalmoscopic  Changes. — Pathological  changes 
in  the  fundus  of  the  eye,  and  particularly  in  the  optic 
nerve,  are  of  frequent  occurrence  in  the  history  of 
structural  disease  of  the  nervous  system.  Many  of  these 
alterations  in  the  optic  nerve  may  be  carefully  studied 
during  life  with  the  aid  of  the  ophthalmoscope,  for  in 
the  optic  disc  we  have  presented  to  direct  view  the 
termination  of  the  optic  nerve.  The  information  thus 
obtained  is  of  the  highest  importance  in  diagnosis,  and 
renders  a  knowledge  of  ophthalmoscopic  technique  in- 
dispensable to  the  student  of  nervous  diseases.  Of  the 
changes  which  are  observed,  some  are  the  direct  conse- 
quence of  the  cerebral  or  spinal  cord  lesion — that  is, 
they  are  consecutive  to  the  process  in  the  nervous  system  ; 
others  are  not  related  directly  to  the  morbid  process  in 
the  nervous  system,  but  to  the  ultimate  cause  of  this  pro- 
cess— that  is,  they  stand  in  the  same  relation  to  this  cause 
as  does  the  process  within  the  nervous  system,  and  are 
hence  denominated  associated  changes.  The  consecutive 
changes  are  optic  neuritis  (or  inflammation  of  the  optic 
nerve)  and  some  forms  of  atrophy  of  the  optic  nerve. 


SYMPTOMATOLOGY    OF   NERVOUS   DISEASES.      169 

In  optic  Neuritis  the  optic  nerve  may  be  inflamed 
throughout  its  entire  extent,  or  the  inflammatory  pro- 
cess may  be  most  marked  in  one  particular  part  of  its 
course.  When  the  inflammation  is  most  intense  behind 
the  eyeball  (retro-bulbar  neuritis),  the  visible  signs  of 
neuritis  may  be  slight  or  absent,  though  there  is  con- 
siderable loss  of  vision.  When  the  inflammation  is  most 
marked  as  it  generally  is,  at  the  optic  papilla  within  the 
globe,  there  are  always  distinctive  ophthalmoscopic  signs 
(papillitis).  At  first  the  disc  becomes  slightly  swollen, 
and  its  edge,  which  is  normally  sharply  defined,  grows 
less  distinct.  This  loss  of  distinctness  or  "  softening  " 
of  the  edge  of  the  disc  is  the  important  characteristic  of 
beginning  papillitis,  the  swelling  of  the  disc  being  at 
first  only  very  slight  and  causing  little  appreciable  pro- 
jection of  the  papilla.  The  nasal  side  of  the  disc  (which 
possesses  more  nerve-fibres  than  the  temporal  side)  is 
generally  the  first  to  grow  indistinct ;  later  the  blurring 
involves  the  entire  circumference  of  the  papilla.  The 
normal  white  central  depression  (physiological  cup)  is 
soon  obliterated,  and  the  whole  disc,  which  at  first  shows 
only  slightly  increased  vascularity,  assumes  a  full  red 
tint,  or  a  grayish  opalescence.  On  direct  examination 
(p.  605^)  the  disc  has  a  distinctly  striated  appearance,  the 
striae  radiating  from  the  centre  of  the  disc  and  corre- 
sponding to  the  course  of  the  nerve-fibres.  Early  in  the 
process  the  vessels  show  little  change  ;  when  the  swelling 
is  marked  the  veins  become  wider  and  tortuous,  and 
maybe  lost  as  they  pass  over  the  edge  of  the  disc.  The 
arteries  may  remain  normal  in  size  ;  frequently  they  are 
contracted.  They  may  be  partially  hidden  from  view  by 
the  opacity.  As  the  papilla  grows  more  and  more  promi- 
nent the  breadth  increases,  until  it  may  attain  twice  the 
diameter  of  a  normal  papilla.     The  prominence  of  the 


170         DISEASES   OF   THE   NERVOUS   SYSTEM. 

disc  is  so  great  in  some  cases  that  it  can  be  distinctly 
seen  with  a  7  D  convex  lens.  A  gradual  subsidence  of 
these  changes  takes  place  after  a  few  weeks  or  months. 
The  opacity  of  the  disc  slowly  disappears  and  the  out- 
lines of  the  papilla  again  become  recognizable,  although 
the  disc  may  continue  for  some  time  to  look  hazy 
(''  woolly  disc  ").  In  slight  degrees  of  neuritis  the  disc 
may  regain  its  normal  appearance.  In  more  severe  cases 
the  papilla  grows  white  or  pale,  and  the  arteries  continue 
narrow  or  grow  even  more  contracted  ;  "consecutive'* 
or  "  post-neuritic  "  atrophy  sets  in. 

The  inflammatory  changes  which  are  seen  with  the  aid 
of  the  microscope  in  the  papilla  can  often  be  observed, 
though  in  less  degree,  throughout  the  course  of  the  optic 
nerve,  and  may  be  traced  through  the  chiasma.  Imme- 
diately behind  the  eyeball  the  space  between  the  inner 
and  outer  sheath  of  the  nerve  is  generally  distended 
with  fluid  inflammatory  products. 

An  intense  grade  of  optic  neuritis  (papillitis)  always 
gives  rise  to  impaired  vision.  The  acuity  of  sight  is 
diminished  and  the  field  of  vision  becomes  restricted 
both  for  white  and  for  colors.  Sometimes  the  impair- 
ment of  vision  is  very  great,  particularly  for  green  and 
red,  but  not  infrequently  it  is  inconsiderable,  even  with 
a  high  grade  of  neuritis.  The  grade  of  visual  disturbance 
is  often  greater  during  the  subsidence  of  the  neuritis 
than  during  the  period  of  most  intense  congestion.  In 
optic  neuritis  of  slight  or  moderate  intensity  there  may 
be  a  corresponding  degree  of  visual  defect,  but  it  is  an 
important  fact  that  even  a  considerable  grade  of  neuritis 
frequently  causes  no  appreciable  disturbance  of  sight. 
We  can  never  exclude  optic  neuritis  because  a  patient 
has  a  high  grade  of  visual  acuity. 

Optic  neuritis  may  occur  in  consequence   of  several 


SYMPTOMATOLOGY    OF  NERVOUS   DISEASES.      I/I 

different  intracranial  processes.  Of  these  causes  tumoi 
is  by  far  the  most  frequent.  The  nature,  size,  and  seat 
of  the  tumor  appear  to  exert  little  influence  in  the  pro- 
duction of  the  neuritis.  The  neuritis  of  tumor  is  often  in- 
tense, and  it  is  of  diagnostic  importance  that  an  intense 
degree  of  neuritis  is  not  often  the  result  of  any  other 
process.  Optic  neuritis  occurs  in  about  nine  tenths  of 
all  intracranial  tumors.  Meningitis  is  the  next  most 
frequent  cause,  and  the  neuritis  is  somewhat  more  fre- 
quent in  meningitis  of  the  base  than  of  the  convexity. 
Cerebral  abscess  (though  less  frequently  a  cause  than 
meningitis)  is  certainly  not  an  infrequent  cause  of  optic 
neuritis.  About  six  per  cent,  of  all  cases  of  multiple 
sclerosis  are  accompanied  with  optic  neuritis,  which  is 
frequently  slight  and  of  short  duration.  In  these  cases 
there  are  inflammatory  or  sclerotic  patches  in  the  optic 
nerve.  In  thrombotic  softening  and  hemorrhage,  optic 
neuritis  is  of  rare  occurence,  but  in  embolic  softening  it 
is  less  uncommon.  Occasionally  optic  neuritis  is  met 
with  in  diffuse  cerebritis.  It  is  also  seen  after  sunstroke 
and  in  idiopathic  hydrocephalus.  The  optic  neuritis  of 
brain  disease  is  almost  always  double,  but  the  process  is 
often  more  advanced  in  one  eye.  In  multiple  sclerosis 
the  neuritis  is  very  often  one-sided,  in  consequence  of 
unilateral  involvement  of  the  nerve  by  a  sclerotic  patch, 
and  it  is  occasionally  one-sided  in  other  forms  of  brain 
disease,  but,  in  general,  unilateral  neuritis  is  much  more 
often  due  to  disease  within  the  orbit  or  at  the  optic 
foramen  than  to  cerebral  processes. 

In  rare  instances  optic  neu  ritis  has  been  developed  in  the 
course  of  acute  or  subacute  disease  of  the  spinal  cord  — 
transverse  and  disseminated  myelitis,  for  example.  It  is 
probable  that  in  most  of  these  cases  the  neuritis  is  to  be  re- 
garded as  an  associated  and  not  as  a  consecutive  process 


1/2         DISEASES   OF   THE   NERVOUS   SYSTEM. 

Not  infrequently  optic  neuritis  occurs  in  consequence 
of  disease  outside  of  the  nervous  system.  It  is  often 
seen  in  the  course  of  chronic  diffuse  nephritis,  and  oc- 
casionally occurs  in  chlorosis,  marked  anaemia,  diabetes, 
lead  poisoning,  scarlet  fever,  typhoid  fever,  and  erysipe- 
las. In  some  of  these  conditions,  notably  in  anaemia, 
lead  poisoning,  and  nephritis,  there  may  be  considerable 
headache,  and  the  association  of  this  with  optic  neuritis 
may  give  rise  to  a  suspicion  of  intracranial  disease,  if 
the  occurrence  of  papillitis  under  these  circumstances  is 
not  borne  in  mind.  Degenerative  changes  are  often 
seen  in  the  retina  in  cases  of  nephritic  optic  neuritis 
(neuro-retinitis).  These  changes  consist  of  small  white 
patches  of  fatty  degeneration,  often  characteristically 
grouped  about  the  macula  lutea.  When  these  changes 
are  present  they  show  the  neuritic  process  to  be  depend- 
ent on  kidney  disease.  Their  absence,  however,  does 
not  by  any  means  exclude  the  possibility  of  the  nephritic 
origin  of  the  neuritis. 

As  regards  the  mechanism  by  which  optic  neuritis  is 
produced,  there  is  still  considerable  difference  of  opin- 
ion, but  it  is  probable  that  the  most  important  single 
factor  is  a  descending  inflammation  along  the  optic  nerve, 
or  along  the  sheath  by  which  it  is  invested.  This  view 
is  supported  by  the  pathological  findings  in  a  large  num- 
ber of  cases  of  optic  neuritis,  and  it  is  the  only  mechanism 
which  will  explain  the  occasional  occurrence  of  unilateral 
optic  neuritis  on  the  side  opposite  a  cerebral  tumor.  Dis- 
tension of  the  optic  sheath  immediately  behind  the  globe 
with  serous  fluid  is  of  frequent  occurrence  in  optic  neu- 
ritis, and  may  be  a  factor  in  heightening  the  inflamma- 
tion of  the  papilla,  by  preventing  the  escape  and  absorp- 
tion of  products  of  inflammation.  It  is  also  possible 
that  this  fluid  may  at  times  contain  irritating  pathogenic 


SYMPTOMATOLOGY    OF   NERVOUS   DISEASES.      173 

material  which  is  capable  of  inducing  a  certain  degree  of 
neuritis.  There  can  be  no  doubt,  however,  that  the  first- 
mentioned  mechanism  is  frequently  alone  effective. 
The  theory  that  increased  intracranial  pressure  is  opera- 
tive in  causing  optic  neuritis  by  causing  pressure  on  the 
cavernous  sinus  is  now  untenable  :  (i)  Because  a  free 
anastomosis  has  been  shown  to  exist  between  the  orbital 
and  facial  veins  ;  (2)  because  large  tumors  of  the  brain 
and  great  hydrocephalus  may  exist  with  little  or  no  neu- 
ritis ;  (3)  because  tumors  so  small  as  to  cause  no  appre- 
ciable change  in  intracranial  pressure  often  produce  a 
high  grade  of  optic  neuritis.  It  is  to  be  regretted  that 
this  theory  once  gained  so  firm  a  hold  that  many  still 
cling  to  it  in  the  face  of  the  objections  mentioned. 

In  the  minds  of  many  there  is  even  at  the  present  day 
a  belief  that  optic  neuritis  is  a  symptom  which  is  of  use 
in  the  localization  of  cerebral  lesions.  This  is  an  error. 
Optic  neuritis  is  usually  a  diffuse  and  not  a  focal  symp- 
tom, and  while  it  is  a  little  more  common  with  lesions 
in  certain  locations  in  the  brain  than  in  others,  the  symp- 
tom possesses  pratically  no  localizing  value. 

Atrophy  of  the  Optic  Nerve. — Several  clinical  varieties 
of  atrophy  of  the  optic  nerve,  of  importance  in  their 
bearing  on  the  diagnosis  of  disease  of  the  central 
nervous  system,  must  be  distinguished.  Primary  or 
simple  atrophy,  that  is,  atrophy  which  is  not  preceded 
by  any  recognizable  inflammatory  change  in  the  papilla 
or  surrounding  structures,  occurs  in  the  degenerative 
diseases  of  the  brain  and  spinal  cord.  It  is  probably  of 
more  frequent  occurrence  in  multiple  sclerosis  and  loco- 
motor ataxia  than  in.  any  other  forms  of  disease.  In 
multiple  sclerosis  it  is  much  more  common,  in  some 
degree,  than  is  generally  supposed.  In  a  small  propor- 
tion of  these  cases  the  atrophy  is  complete  ;  in  a  consid- 


174         DISEASES   OF   THE   NERVOUS   SYSTEM. 

erable  proportion  (about  20  per  cent.)  the  atrophy  Is 
partial,  but  involves  the  whole  papilla,  and  in  nearly  the 
same  number  of  cases  the  atrophic  change  is  partial  and 
involves  only  the  temporal  half  of  the  disc.  In  loco- 
motor ataxia,  optic  atrophy  is  present  in  about  15  per 
cent,  of  all  cases,  and  is  frequently  an  early  symptom. 
The  form  of  atrophy  is  rather  characteristic,  the  disc 
being  usually  gray,  as  seen  by  the  ophthalmoscope,  with 
little  or  no  diminution  in  the  size  of  the  vessels, — ''  gray 
atrophy."  In  a  closely  allied  disease,  dementia  paralyt- 
ica, optic  atrophy  occurs  in  a  small  proportion  of  cases 
(5  per  cent.),  but  here,  as  in  multiple  sclerosis,  the 
atrophy  is  probably  to  be  regarded  as  an  associated  and 
not  as  a  consecutive  change. 

Primary  atrophy  also  occurs  unassociated  with  central 
disease.  Such  atrophy  has  been  attributed  to  cold, 
menstrual  disturbance,  migraine,  exhausting  diarrhoeas, 
and,  very  rarely,  to  diabetes,  syphilis,  and  various  spe- 
cific diseases.  Tobacco,  alcohol,  and  lead  may  lead  to 
partial  atrophy,  but  this  is  frequently  preceded,  in  the 
case  of  tobacco  and  alcohol,  by  an  axial  neuritis. 
Primary  atrophy  generally  involves  both  eyes,  but  one  is 
often  involved  much  earlier  than  the  other.  Not  very 
rarely  one  eye  alone  is  affected. 

Disease  of  the  optic  nerve  behind  the  eye  or  at  the 
chiasm  may  cause  atrophy  (usually  gray)  of  the  optic 
nerve.  Occasionally  such  atrophy  is  preceded  by  slight 
neuritis  ;  usually  it  is  not.  This  form  is  denominated 
"  secondary  atrophy."  Loss  of  sight  generally  precedes 
visible  signs  of  atrophy  by  a  considerable  period, 

Neuritic  or  papillilic  atrophy  is  that  variety  which 
follows  optic  neuritis.  Frequently,  but  by  no  means 
always,  the  neuritis  leaves  changes  in  the  choroid  and  in 
the  vessels   which  make  it  possible  to  distinguish  neuritic 


SYMPTOMATOLOGY    OF   NERVOUS   DISEASES.      175 

atrophy  from  the  simple  form.  Another  variety  of 
atrophy  is  that  which  occurs  after  disease  of  the  choroid 
and  retina. 

The  ophthalmoscopic  appearances  of  atrophy  vary 
somewhat  in  different  cases.  In  all  cases  the  disc  is 
whiter  than  normal,  but  the  degree  and  character  of  the 
pallor  presents  differences.  The  pallor  may  affect  the 
whole  disc  or  its  temporal  side  only.  But  the  temporal 
side  of  the  disc  is  normally  somewhat  pale,  because  the 
nerve-fibres  are  there  least  numerous,  and  this  may  give 
rise  to  some  difficulty  in  diagnosis  when  the  pallor  of 
atrophy  is  confined  to  the  temporal  side  of  the  papilla. 
The  pallor  of  atrophy  is  due  to  the  wasting  of  the  capil- 
laries of  the  disc  which  accompanies  the  degeneration  of 
the  nerve-fibres.  The  tint  of  the  disc  varies,  being  in 
some  cases  milk-white,  in  others  grayish,  and  in  others 
bluish  or  yellowish.  There  is  no  diminution  in  the  size 
of  the  optic  disc  in  atrophy,  because,  although  the  nerve 
usually  shrinks,  the  size  of  the  papilla  is  dependent  on  the 
size  of  the  sclerotic  opening.  Frequently  the  edge  of  the 
disc  becomes  very  sharp  and  distinct.  Sometimes  the  ves- 
sels are  diminished  in  size,  but  this  is  not  a  constant  change. 

When  optic  atrophy  is  pronounced  there  is  some 
diminution  in  the  acuity  of  vision.  In  general,  the  degree 
of  visual  loss  is  related  to  the  degree  of  visible  change 
(pallor)  in  the  optic  nerve,  but  to  this  rule  there  are 
important  exceptions.  In  some  cases  there  is  a  high 
degree  of  visual  defect  with  little  or  no  pallor.  When  it 
is  remembered  that  the  whiteness  of  the  disc  depends  on 
wasting  of  the  capillaries,  while  the  visual  loss  depends 
directly  on  the  degree  of  change  on  the  nerve-fibres -of 
the  optic  nerve,  it  is  not  surprising  to  find  that  there  is 
not  infrequently  a  want  of  correspondence  between 
visual  acuity  and  the  tint  of  the  papilla. 


176        DISEASES   OF  THE   NERVOUS   SYSTEM. 

The  visual  field,  both  for  colors  and  for  white,  shows 
some  degree  of  peripheral  limitation  in  almost  all  cases 
of  atrophy.  In  some  cases  this  limitation  is  concentric, 
in  others  sector-like.  Impaired  color-vision  is  another 
accompaniment  of  optic  atrophy,  which,  in  some  degree, 
is  present  in  a  large  proportion  of  cases.  Green  is 
usually  the  color  first  lost  ;  red  the  next 

Of  the  Associated  Ophthalmoscopic  Changes  of  importance 
in  relation  to  nervous  disease,  the  following  are  the  prin- 
cipal : 

1.  Primary  atrophy  of  the  optic  nerve,  occurring  for 
the  most  part  in  association  with  degenerative  diseases 
of  the  brain  and  spinal  cord. 

2.  Albuminuric  retinitis  is  of  importance,  because  it 
is  so  frequently  associated  with  atheromatous  change  in 
the  arteries,  and  such  degeneration  may  lead  either  to 
cerebral  hemorrhage  or  to  thrombotic  softening. 

3.  Syphilitic  choroiditis  and  the  atrophy  which  follows 
it  are  frequently  seen  in  brain  disease  from  acquired 
and  sometimes  from  congenital  syphilis.  Certain  forms 
of  atrophy  of  the  choroid,  however,  result  from  other 
conditions  than  syphilis  (posterior  staphyloma,  hemor- 
rhage, senile  change). 

4.  Tubercles  of  the  choroid  are  in  rare  cases  met  with 
in  tubercular  meningitis.  They  are  much  less  frequently 
observed  when  there  is  tubercular  meningitis  only  than 
when  such  meningitis  is  associated  with  general  tuber- 
culosis. When  they  develop  early  in  the  disease  they 
may  be  of  the  greatest  assistance  in  diagnosis. 

5.  Embolism  of  the  central  artery  of  the  retina  very 
rarely  occurs  in  cases  of  cerebral  embolism. 

6.  Retinal  hemorrhages  occur  under  a  variety  of  con- 
ditions— in  albuminuria,  leucocythaemia,  purpura,  etc. 
Occasionally    small    hemorrhages    are    found    in     the 


SYMPTOMATOLOGY    OF   NERVOUS   DISEASES.      J// 

meninges,  particularly  the  pia  mater,  in  these  conditions, 
but  they  generally  give  rise  to  no  symptoms. 

The  routine  use  of  the  ophthalmoscope  in  all  cases  of 
nervous  disease  in  which  there  is  even  a  possibility  of 
discovering  changes  in  the  fundus  cannot  be  too  strongly 
urged.  It  is,  however,  important  to  remember  that  the 
condition  of  the  circulation  within  the  eye  is  not  in  any 
sense  an  index  of  the  condition  of  the  circulation  within 
the  cranial  cavity. 

Auditory  Symptoms. — Deafness  of  nervous  origin, 
that  is,  due  to  disease  of  the  terminal  auditory  filaments 
in  the  labyrinth,  or  to  disease  of  the  auditory  nerve  or  its 
central  connections  (p.  67),  is  of  relatively  uncommon 
occurrence  as  compared  with  deafness  from  middle-  and 
external-ear  disease.  The  character  of  such  *'  nervous 
deafness  "  is  the  same,  whether  the  disease  causing  it  be 
central  or  peripheral  ;  there  is  defective  conduction  of 
sound  through  the  cranial  bones  d.^  well  as  through  the  air. 
This  constitutes  a  sharp  distinction  from  the  deafness 
dependent  on  disease  of  the  middle  and  external  ear, 
which  impairs  the  perception  of  sounds  conducted 
through  the  air,  while  it  does  not  destroy  the  ability  to 
perceive  sounds  conducted  through  the  cranial  bones. 
In  making  use  of  this  method  of  distinguishing  between 
deafness  due  to  disease  of  nervous  structures  and  that 
dependent  on  middle-  or  external-ear  disease,  either  a 
vibrating  tuning-fork  or  a  watch  may  be  employed.  In 
persons  more  than  fifty  years  of  age  it  is  not  rare  to  find 
some  diminution  in  the  perception  of  vibrations  trans- 
mitted through  the  bones  of  the  skull,  owing  to  changes 
in  the  labyrinth  incidental  to  the  degenerative  period  of 
life.  This  diminution  is  bilateral  and  never  amounts  to 
complete  loss,  though  frequently  the  ticking  of  a  watch 
is  no  longer  perceived  when  the  latter  is  in  contact  with 
the  zygoma. 


1/8         DISEASES   OF  THE   NERVOUS   SYSTEM. 

Since  the  character  of  the  deafness  is  the  same,  whether 
it  be  due  to  labyrinthine,  nerve,  or  central  disease,  the 
localization  of  the  situation  of  the  disease  depends  on 
associated  symptoms.  If  there  is  paralysis  of  the  facial 
nerve  on  the  same  side  as  the  deafness,  and  there  is  no 
middle-ear  or  bone  disease,  the  lesion  is  certainly  in  the 
auditory  nerve,  either  within  the  auditory  canal  or  be- 
tween this  and  the  superficial  origin  of  the  nerve  from 
the  upper  part  of  the  medulla.  If  deafness  of  rapid  or 
sudden  onset  is  associated  with  symptoms  of  medullary 
or  pontine  disease,  especially  with  hemiplegia  on  the  side 
opposite  the  loss  of  hearing,  the  lesion  probably  involves 
the  auditory  nucleus  (p.  55).  Deafness  associated  with 
hemiansesthesia  or  hemiplegia  on  the  same  side  probably 
indicates  disease  of  the  internal  capsule  or  extensive 
cortical  disease  involving  the  auditory  centre  in  the  first 
temporo-sphenoidal  convolution.  Deafness  from  disease 
involving  this  centre  is  exceedingly  rare. 

Much  the  most  frequent  cause  of  nervous  deafness, 
both  unilateral  and  bilateral,  is  labyrinthine  disease. 
Such  disease  also  gives  rise  to  tinnitus  and  frequently  to 
vertigo,  and  the  association  of  one  or  both  of  these  con- 
ditions with  nervous  deafness  suggests,  but  does  not 
prove,  the  existence  of  disease  of  the  labyrinth.  It  does 
Tio\. prove  its  existence  because  disease  of  the  nerve  may 
have  the  same  association,  but  in  this  case  there  is  usually 
evidence  of  other  nerve  disease  (facial  paralysis).  The 
nature  of  the  labyrinthine  disease  varies  in  different 
cases.  Acute  and  chronic  inflammation,  syphilitic  dis- 
ease, and  degenerative  processes  occur.  The  deafness 
produced  by  certain  drugs  (quinine,  etc.)  is  probably  of 
labyrinthine  origin. 

The  auditory  nerve  suffers  chiefly  from  processes 
originating  in  neighboring  structures — meningitis,  simple 
and  syphilitic,  new  growths,  etc. 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      1/9 

Disease  involving  the  auditory  nuclei  is  generally 
softening  or  hemorrhage,  sometimes  tumor. 

Disease  of  the  auditory  path  above  the  nuclei,  in  the 
tegmentum  of  the  crus,  in  the  internal  capsule,  or  in  the 
white  substance  of  the  temporo-sphenoidal  lobe,  is  rare. 

Occasionally  deafness  is  of  functional  origin.  It  is 
not  uncommon  in  hysteria  in  association  with  hemian- 
aesthesia,  etc. 

Tinnitus  Aurium  is  a  term  used  to  designate  all  sounds 
which  are  referred  to  the  ear,  and  have  no  objective 
cause  external  to  the  body.  These  subjective  sounds,  as 
described  by  patients,  are  exceedingly  varied  in  charac- 
ter. Generally  they  are  simple  in  nature — that  is,  of  a 
low  degree  of  elaboration,  and  are  spoken  of  as  **  sing- 
ing," "  ringing,"  "  hissing,"  '"'buzzing,"  "  whistling,"  etc. 
Sometimes  they  are  more  elaborate  in  character,  and  are 
compared  to  the  ringing  of  bells,  the  rustling  of  wand  in 
the  trees,  etc.  The  simpler  sounds  may  be  either 
aural  or  central  in  origin,  but  those  of  greater  elabora- 
tion are  almost  always  of  central  (cortical)  origin.  The 
sound  may  be  constant  or  intermittent,  continuous  or 
pulsatory.  In  intracranial  aneurism  (carotid  or  verte- 
bral) a  pulsating  sound  has  in  very  rare  instances  been 
produced,  which  could  be  heard  by  another  person,  and 
such  a  sound,  if  audible  on  auscultation,  makes  the  exist- 
ence of  aneurism  highly  probable,  and  practically  certain 
if  there  are  at  the  same  time  evidences  of  a  tumor  at  the 
base  of  the  brain.  But  though  the  diagnostic  significance 
of  this  sign  is  great,  its  extreme  rarity  makes  it  of  little 
practical  use. 

In  the  great  majority  of  cases  tinnitus  is  of  aural 
origin,  for  nearly  all  diseases  of  the  ear,  inner,  middle, 
or  outer,  may  be  accompanied  by  it.  Much  less  fre- 
quently  the    cause  is   organic   irritative   disease   of  the 


l8o         DISEASES   OF   THE   NERVOUS   SYSTEM. 

auditory  nerve  or  centre  Functional  derangement  of 
the  cortical  auditory  centres  occasionally  gives  rise  to 
tinnitus.  Thus,  an  epileptic  attack  may  be  preceded  by  a 
paroxysmal  sound,  due  no  doubt  to  nervous  discharge 
from  the  nerve-cells  constituting  the  auditory  centre, 
and  very  rarely  such  sounds  occur  in  migraine.  Occa- 
sionally a  continuous  tinnitus  occurs  in  cases  of  neuras- 
thenia, mental  depression,  etc.  Intense  habitual  stimu- 
lation of  the  auditory  nerve,  as  by  the  sound  of  cannon, 
musical  instruments,  etc.,  may  cause  tinnitus. 

Usually  some  degree  of  deafness  coexists  with  tin- 
nitus. When  this  is  the  case  both  deafness  and  tinnitus 
are  dependent  on  the  same  cause,  and  what  this  cause  is 
must  be  determined  by  a  study  of  the  associated  symp- 
toms, as  already  mentioned  in  speaking  of  deafness. 

Vertigo. — This  word  has  been  loosely  used  to  desig- 
nate almost  any  subjective  sensation  that  is  associated 
with  a  feeling  of  imperfect  equilibrium,  or  of  transient 
mental  confusion.  When  correctly  used,  the  term  is 
applied  only  to  sensations  in  which  there  is  experienced 
a  feeling  of  movement,  often  of  turning,  or  in  which 
surrounding  objects,  which  are  really  at  rest,  have  the 
appearance  of  moving  in  a  definite  direction.  These 
subjective  sensations  are  often  accompanied  by  a  com- 
pensatory movement  of  the  body  of  the  patient,  which 
may  result  in  a  fall.  Some  impairment  of  conscious- 
ness, never  amounting  to  actual  loss,  always  exists  in 
vertigo. 

Vertigo  is  a  frequent  symptom  of  organic  brain  dis- 
ease, but  it  is  a  much  more  common  symptom  of  periph- 
eral disturbance.  Occasionally  it  occurs  where  there 
is  no  discoverable  cause  for  it,  and  then  it  is  sometimes 
termed  "  essential  "  vertigo.  It  is,  however,  never  to  be 
regarded  as  a  definite  disease,  but  always  as  a  symptom, 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      l8l 

although  in  many  caSes  it  is  the  most  obtrusive  symptom 
of  the  condition  on  which  it  depends. 

Before  mentioning  the  varieties  of  vertigo,  it  is  desira- 
ble to  consider  briefly  the  manner  in  which  the  equi- 
librium of  the  body  is  maintained.  When  the  body  is  in 
any  position  requiring  the  active  contraction  of  muscles 
for  the  maintenance  of  its  balance,  the  centrifugal  motor 
impulses  which  leave  the  brain  for  the  establishment  of 
this  balance  are  influenced  through  the  mediation  of 
cerebral  centres  by  certain  sensory  impressions  which 
serve  for  the  guidance  of  these  centres  in  adapting  the 
position  of  the  body  to  its  environment.  The  most 
important  of  these  sensory  impressions  are  those  derived 
from  the  semicircular  canals  and  from  the  motor  nerves 
of  the  eyeball.  Other  impressions  that  furnish  the 
brain  with  guiding  information  as  to  the  relation  of  the 
body  with  surrounding  objects  are  derived  from  the  skin 
of  those  parts  which  are  in  contact  with  external  things, 
and  from  the  muscles  whose  activity  determines  posture. 
If  any  one  of  these  different  kinds  of  guiding  sensory 
impressions  becomes  imperfect  or  deranged  its  expression 
in  consciousness  is  felt  as  a  derangement  of  the  cerebral 
centre — that  is,  as  vertigo.  Derangement  of  the  aural 
impressions  gives  rise  to  aural  vertigo,  derangement  of 
the  guiding  impressions  of  the  muscles  of  the  eyeball 
results  in  ocular  vertigo. 

Aural  Vertigo — that  is,  vertigo  dependent  on  disease  of 
the  semicircular  canals — is  by  far  the  commonest  and 
most  important  variety  of  vertigo,  constituting  at  least 
nine  tenths  of  all  cases  of  true  vertigo.  The  disease 
of  the  semicircular  canals  is  usually  evidenced  by 
tinnitus  aurium  and  by  nervous  deafness.  Often  the 
latter  is  slight.  Sudden  lesions  of  the  labyrinth  generally 
give  rise  to  violent  attacks  of  vertigo   and  marked  audi- 


l82         DISEASES   OF   THE   NERVOUS   SYSTEM. 

tory  disturbance,  and  this  variety  of  aural  vertigo  is 
properly  known  as  Meniere's  disease,  although  this  name 
is  sometimes  made  to  include  slighter  forms  of  the  affec- 
tion. It  is  common  for  aural  vertigo  to  be  mistaken 
for  evidence  of  organic  disease  of  the  brain,  particu- 
larly for  hemorrhage  and  softening. 

Ocular  Vertigo  is  a  rare  and  usually  slight  form  of 
vertigo  which  is  due  to  paresis  of  an  ocular  muscle. 
The  vertigo  depends  on  the  erroneous  projection  of 
objects  caused  by  the  diplopia  resulting  from  the  pare- 
sis. The  occurrence  of  diplopia  makes  the  diagnosis  of 
the  trouble  easy. 

Vertigo  is  not  infrequently  associated  with  dyspepsia, 
and  the  occurrence  of  vertigo  in  connection  with  gastric 
symptoms  has  led  to  the  description  of  what  is  called 
gastric  vertigo.  It  is  doubtful  whether  vertigo  is  ever 
really  referable  entirely  to  gastric  disorder.  The  ma- 
jority of  the  cases  described  as  gastric  vertigo  are  due  to 
labyrinthine  disturbance  and  are  really  varieties  of  aural 
vertigo.  But  frequently  the  evidences  of  labyrinthine 
trouble  are  slight,  and  the  true  character  of  the  disorder 
is  readily  overlooked.  It  must  not  be  supposed,  how- 
ever, that  gastric  disorder  has  no  influence  in  bringing 
about  vertiginous  attacks.  It  is  easy  to  understand  how 
a  disordered  stomach  may  act,  through  the  central  con- 
nections of  the  vagus,  as  an  important  exciting  cause  of 
vertigo,  by  disturbing  the  balance  of  an  already  unstable 
cerebral  centre. 

Vertigo  sometimes  constitutes  an  aura  of  the  seizures  of 
petit  mal,  and,  at  times,  of  grand  mal.  The  distinction  of 
this  form  from  aural  vertigo  is  described  on  page  582. 
The  convulsions  of  organic  disease  of  the  brain  are  also 
at  times  preceded  by  vertigo.  As  a  symptom  of  organic 
brain  disease,  vertigo  has  little  diagnostic  significance, 


SYMPTOMATOLOGY    OF   NERVOUS    DISEASES.      183 

for  it  may  occur  in  connection  with  a  variety  of  lesions. 
It  is  especially  frequent  in  lesions  of  the  cerebellum  and 
pons,  and  disease  of  the  middle  peduncle  of  the  cerebel- 
lum gives  rise  not  only  to  vertigo,  but  to  an  actual  forced 
rotation  in  the  long  axis  of  the  body  towards  the  side  of 
the  lesion.  The  mere  occurrence  of  vertigo,  however,  is 
of  no  localizing  value,  as  it  may  be  produced  by  disease 
in  almost  any  part  of  the  brain.  It  may  occur  in  the 
course  of  cerebral  tumor,  abscess,  chronic  meningitis, 
general  paralysis,  multiple  sclerosis,  and  at  the  onset  of 
cerebral  hemorrhage,  embolism,  or  thrombosis. 

When  vertigo  is  severe  it  is  apt  to  be  accompanied  by 
vomiting,  which  seems  to  be  entirely  dependent  on  the 
severity  of  the  vertigo  and   not  upon  its  cause. 

Slight  vertiginous  attacks,  consisting  merely  in  a  sense 
of  defective  equilibrium,  may  occur  in  the  course  of  hys- 
teria, neurasthenia,  anaemia,  etc. 

Gustatory  Symptoms. — The  more  important  facts 
relating  to  loss  of  taste  have  already  been  sufficiently  con- 
sidered in  connection  with  the  anatomy  of  the  fifth  nerve 
(p.  61).  There  remain  to  be  mentioned  only  the  per- 
version of  the  sense  of  taste  (parageusia)  which  is 
occasionally  observed  in  hysteria,  insanity,  and  other 
neuroses  ;  the  increased  sensitiveness  of  taste,  which  is 
of  occasional  occurrence,  under  the  same  conditions  ;  and 
the  various  subjective  sensations  of  taste,  usually  un- 
pleasant in  character,  that  occur  in  insanity,  and,  rarely, 
as  the  aura  of  an  epileptic  paroxysm.  With  the  possible 
exception  of  aurae  of  taste  these  disturbances  are  of  slight 
diagnostic  importance. 

Trophic  Symptoms. — The  nutrition  of  the  various 
tissues  of  the  body  is  to  a  considerable  extent  under  the 
domination  of  nervous  structures,  but  we  know  little  oi 
the  exact  character  of  this  influence  and  of  the  conditions 


l84        DISEASES   OF   THE   NERVOUS    SYSTEM. 

on  which  it  depends.  In  the  case  of  certain  tissue  ele- 
ments the  changes  in  nutrition  that  result  from  morbid 
conditions  of  the  nervous  system,  in  consequence  of  this 
dependence,  are  very  striking  and  possess  considerable 
diagnostic  significance.  The  principal  structures  in  which 
such  alterations  occur  are  the  skin,  the  bones  and  joints, 
and  the  muscles. 

Trophic  Changes  in  the  Skin  may  result  from  peripheral, 
spinal,  or  cerebral  lesions.  They  vary  considerably  in 
character  according  to  the  acuteness  of  the  lesion  which 
gives  rise  to  them,  and  are  much  more  marked  and  frequent 
in  peripheral  and  spinal  than  in  cerebral  disease.  When 
the  changes  are  rapid  and  intense,  as  they  are  in  acute 
disease  of  the  nerves  (for  example,  acute  neuritis),  or 
spinal  cord  (acute  myelitis),  the  skin  becomes  hot  and  red, 
bullae  form,  and  slight  pressure  may  give  rise  to  slough- 
ing. In  chronic  lesions  of  the  nerves  and  cord  (chronic 
myelitis,  syringomyelia)  there  is  a  gradual  change  in  the 
nutrition  of  the  skin,  which  grows  thin,  red,  and  glossy, 
and  the  nails  become  retarded  in  growth,  brittle,  and  thick. 
In  chronic  cerebral  disease  (hemorrhage,  softening,  etc.) 
the  skin  sometimes  becomes  rough,  dry,  and  thick,  and 
the  nails  occasionally  grow  curved  and  brittle.  In  general, 
it  may  be  said  that  the  most  serious  trophic  changes  in  the 
skin  take  place  when  the  gray  substance  of  the  cord  or 
posterior  nerve-roots  are  involved  in  irritative  processes-, 
and  there  can  be  little  doubt  that  the  nutrition  of  the  skin 
is  dependent  on  fibres  which  pass  through  the  posterior 
nerve-roots.  There  are  no  special  trophic  nerve-fibres. 
The  situation  of  the  trophic  centres  is  also  obscure, 
but  it  is  probable  that  the  posterior  root-ganglia  are 
in  some  way  related  to  the  nutrition  of  the  skin. 

One  form  of  eruption  is  unquestionably  dependent  on 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.       185 

a  nervous  lesion :  the  eruption  of  herpes  zoster.  There 
is  reason  to  believe  this  affection  to  be  dependent 
on  an  inflammatory  process  involving  one  or  more  in- 
tervertebral ganglia,  a  nerve-trunk  or  its  terminal  nerve- 
filaments. 

It  is  very  possible  that  other  forms  of  eruption  (psoria- 
sis, scleroderma)  are  dependent  on  nervous  lesions,  and 
several  varieties  of  cutaneous  ulceration  (bed-sores  of 
myelitis,  perforating  ulcer  of  foot)  have  long  been  re- 
garded as  true  trophic  lesions.  But  it  is  probable  that  in 
the  case  of  these  ulcerations  the  death  of  tissue  is  caused 
by  external  agencies,  such  as  injuries  and  micro- 
organismic  infection,  which  is  rendered  possible  by  the 
anaesthesia  that  exists  in  these  cases.  Probably  in  ad- 
dition to  the  anaesthesia,  the  nervous  lesion  causes,  in 
these  cases,  some  modification  of  the  nutrition  of  the  parts, 
which  predisposes  them  to  necrosis  from  trivial  injuries. 

The  trophic  changes  that  occur  in  the  eyeball  in  con- 
sequence of  disease  of  the  trigeminus  may  be  mentioned 
in  this  connection.  Lesions  of  the  trigeminus,  partic- 
ularly irritative  lesions  involving  the  first  division  (oph- 
thalmic) of  the  nerve,  are  frequently  followed  by  ulceration 
of  the  cornea  and  subsequent  perforation.  This  is  espe- 
cially apt  to  occur  when  the  lesion  involves  the  Gasserian 
ganglion,  or  the  nerve  in  front  of  it.  Whether  these 
alterations  in  the  nutrition  of  the  eyeball  are  to  be 
regarded  as  true  trophic  changes,  or  simply  as  conse- 
quences of  injuries  which  the  accompanying  anaesthesia 
makes  it  difficult  to  guard  against,  cannot  be  positively 
stated.  It  is  certainly  true  that  under  strict  antiseptic 
care,  ulcers  of  the  cornea  can  be  made  to  heal  rapidly 
and  perfectly,  while  the  nerve-lesion  continues  in  progress. 

Trophic  changes  in  the  Bones  and  Joints  are  observed 
in  the  course  of  spinal  cord  and  cerebral  disease.     Retar- 


I86         DISEASES   OF   THE   NERVOUS   SYSTEM. 

dation  in  the  growth  of  the  bones,  without  pathological 
changes  in  their  histology,  occurs  in  children  when  the 
ganglion-cells  of  the  anterior  horns  are  the  seat  of  acute 
inflammation,  and  in  most  cases  of  hemiplegia  coming  on 
in  the  course  of  childhood.  In  rare  instances  similar 
changes  occur  after  peripheral  nerve-lesions.  Extreme 
atrophy  of  the  bones,  together  with  atrophy  of  the  skin 
and  subcutaneous  tissue,  occurs  in  the  rare  condition 
known  as  progressive  facial  atrophy  (facial  hemiatrophy). 
The  affection  is  strictly  unilateral,  and  probably  depends 
on  some  derangement  in  the  trophic  function  of  the  fifth 
nerve,  possibly  on  disease  of  its  trophic  root  (see  Fig. 
44).  Brittleness  of  the  bones  {fragilitas  ossium)  lead- 
ing to  fracture  from  slight  injuries,  so-called  "spon- 
taneous "  fracture,  is  occasionally  observed  in  dementia 
paralytica,  amyotrophic  lateral  sclerosis,  and  locomotor 
ataxia.  It  is  a  question  whether  the  fragility  in  these 
cases  is  due  directly  to  the  nervous  lesion,  or  is  merely 
one  consequence  of  defective  general  nutrition. 

Inflammation  in  the  larger  joints  is  occasionally  met 
with  in  acute  cerebral  and  spinal-cord  diseases.  The  cer- 
ebral affection  with  which  this  change  is  associated  is 
usually  hemorrhage  or  softening  (the  latter  more  fre- 
quently), and  the  joint  changes  are  limited  to  the  hemi- 
plegic  side.  The  synovitis  comes  on  in  the  course  of  a 
few  weeks  after  the  onset  of  the  hemiplegia.  Bilateral 
effusion  into  the  knee-joints  is  occasionally  observed  in 
the  course  of  acute  myelitis.  Extensive  changes  in  the 
larger  joints  (knee,  shoulder,  elbow)  are  sometimes  ob- 
served in  the  course  of  locomotor  ataxia  ("  spinal  arthro- 
pathies," Charcot's  joint  disease).  These  changes  consist 
of  rather  sudden  and  painless  swelling  of  the  affected 
joint,  loUowed  by  destructive  disease  ot  the  articulation 
itself, — erosion   of    the  cartilage,    atrophy  of    the  heads 


SYxMPTOMATOLOGY   OF  NERVOUS   DISEASES.       187 

of  the  bones,  and  relaxation  of  the  ligaments.  Some- 
times there  are  irregular  osteophytic  growths  external 
to  the  articulation.  At  times  these  changes  appear  to 
be  related  to  slight  injury.  Their  painless  character  is 
an  important  diagnostic  feature  of  these  arthropathies. 
When  these  changes  involve  the  tarsal  articulation,  the 
foot  may  become  flat  {"  tabetic  foot "). 

Trophic  Changes  in  the  Muscles.  The  trophic  changes 
that  occur  in  muscles  exceed  in  diagnostic  importance  all 
other  nutritive  changes  dependent  on  nervous  disease. 
The  diagnostic  indications  are  derived,  first,  from  changes 
in  the  bulk  and  consistence  of  the  muscles,  and,  secondly, 
from  alterations  in  their  electrical  excitability. 

Muscular  Atrophy  is  a  frequent  consequence  of  organic 
disease  of  the  brain,  spinal  cord,  and  peripheral  nerves, 
but  a  high  degree  of  wasting  is  seen  only  in  disease  in- 
volving the  lower  segment  of  the  motor  path — that  is,  in 
disease  of  the  motor  ganglion-cells  of  the  anterior  horns, 
the  anterior  nerve-roots,  or  the  motor  nerves.  Such  a 
degree  of  wasting  may  follow  acute  lesions,  or  may  occur 
in  the  course  of  those  that  are  chronic  in  their  progress. 
In  the  former  case  the  atrophy  is  preceded  by  motor  par- 
alysis of  sudden  or  rapid  onset  (acute  poliomyelitis,  acute 
myelitis,  acute  neuritis,  injuries  to  motor  nerves)  ;  in  the 
latter,  the  paralysis  progresses  pari  passu  with  the  weak- 
ness, being  due  to  the  gradual  wasting  of  muscular  tissue 
(progressive  muscular  atrophy).  In  an  important  group 
of  cases  of  muscular  atrophy  of  gradual  development,  in 
which  no  constant  changes  in  the  spinal-cord  or  periph- 
eral nerves  have  yet  been  detected,  and  which  are 
looked  upon  as  myopathic  in  origin  (progressive  muscu- 
lar dystrophies — idiopathic  muscular  atrophy),  a  high  de- 
gree of  muscular  wasting  is  frequently  observed.  These 
cases  constitute  the  only  exception  to  the  rule  that  a  high 


l88         DISEASES    OF   THE   NERVOUS   SYSTEM. 

grade  of  muscular  atrophy  is  due  to  anterior  cornual  or 
peripheral  nerve  disease.  Their  distinction  from  forms 
of  atrophy  dependent  on  nervous  lesions  is  considered 
elsewhere. 

It  must  not  be  supposed  that  all  cases  of  disease  of 
the  anterior  cornua,  or  motor  nerves,  are  productive  of  a 
high  degree  of  muscular  wasting.  In  lesions  of  moderate 
severity  or  of  gradual  onset  the  wasting  may  be  moderate 
or  slight  in  degree,  and,  unless  the  distribution  be  dis- 
tinctive, may  resemble  that  which  occurs  after  cerebral 
lesions.  The  atrophy  which  follows  disease  of  the  upper 
segment  of  the  motor  path  (cerebral  disease,  many  forms 
of  spinal-cord  disease  not  involving  the  anterior  cornua) 
is  usually  slight  in  degree  ;  occasionally  it  is  considerabl'^, 
but  it  never  reaches  the  grade  commonly  observed  in  dis- 
ease of  the  lower  segment  (myelitis,  progressive  muscular 
atrophy,  multiple  neuritis). 

The  rapidity  with  which  muscular  atrophy  develops 
varies  greatly  under  different  circumstances.  In  disease 
of  the  lower  segment  of  the  motor  path  the  rapidity  of 
wasting  depends  chiefly  on  the  acuteness  or  chronicity  of 
the  lesion  to  which  it  is  due.  In  acute  processes  the 
wasting  progresses  with  rapidity,  often  reaching  a  high 
degree  in  the  course  of  a  month,  and  often  being  readily 
appreciable  after  the  lapse  of  ten  days  (acute  myelitis, 
acute  poliomyelitis).  In  gradually  progressive  lesions 
the  atrophy  is  proportionately  slow. 

Disease  involving  the  upper  segment  of  the  motor  path 
is  generally  followed  by  some  muscular  atrophy,  but  this  is 
•almost  invariably  late  in  its  development.  This  atrophy  is 
particularly  noticeable  in  young  subjects  and  is  frequently 
a  result  of  irritative  lesions.  In  a  very  small  proportion 
of  cases,  cerebral  lesions,  especially  disease  of  the  cortex 
and  subjacent  white  substance,  are  followed  not  by  late 
but  by  early  atrophy — atrophy  which  reaches  its  height 


SYMPTOMATOLOGY   OF   NERVOUS    DISEASES.       189 

in  from  three  to  six  weeks  after  the  onset  of  the  lesion, 
which  is  generally  irritative  in  character.  These  early- 
cerebral  atrophies  are  mainly  observed  during  adoles- 
cence and  during  early  adult  life.  Usually  the  degree  of 
wasting  is  inconsiderable.  Both  late  and  early  atrophies 
are  probably  dependent,  in  a  measure,  on  secondary  de- 
generation of  the  pyramidal  tracts,  which,  when  due  to 
irritative  processes,  seems  to  exert  a  detrimental  influ- 
ence on  the  nutrition  of  the  ganglion-cells  of  the  anterior 
horns  and  through  these  on  the  muscles.  In  rare  in- 
stances hypertrophy  of  paralyzed  parts  may  occur,  which 
is,  as  yet,  without  satisfactory  explanation. 

In  disease  of  the  lower  segment  of  the  motor  path  the 
muscles  usually  become  flabby  and  lose  their  tone  ;  they  un- 
dergo "  atonic  atrophy."  In  disease  of  the  upper  segment 
the  muscles  may  retain  their  tone,  or,  if  there  be  well-devel- 
oped secondary  degeneration  of  the  pyramidal  tracts  and 
increased  reflex  action,  may  grow  hypertonic  and  exhibit 
muscular  rigidity.  When  there  is  secondary  degeneration 
of  the  pyramidal  tracts,  muscular  rigidity  may  be  pre- 
served in  cases  of  atrophy  from  disease  of  the  ganglion- 
cells  of  the  anterior  horns,  provided  some  of  the  ganglion- 
cells  of  the  anterior  cornua  are  only  partially  damaged, 
and  still  exert  enough  control  over  the  muscular  tone  to 
cause  that  over-action  which  develops  under  the  influence 
of  degeneration  in  the  upper  segment  of  the  motor  path. 
If,  however,  the  ganglion-cells  of  the  anterior  cornua  are 
so  extensively  diseased  as  to  abolish  the  muscular  tonus, 
the  degeneration  of  the  upper  segment  is  incapable  of 
causing  rigidity. 

The  distribution  of  the  atrophy  corresponds  closely 
with  the  distribution  of  the  motor  paralysis  in  cases  where 
the  wasting  follows  such  paralysis.  In  cases  where  the 
wasting  is  not  secondary  in  time  or  causation  to  motor 


190         DISEASES   OF   THE  NERVOUS   SYSTEM. 

paralysis,  the  distribution  of  atrophy  presents  considerable 
variety  and  forms  a  basis  for  the  distinction  of  clinical 
types. 

True  Muscular  Hypertrophy  rarely  occurs  as  a  phenome- 
non of  disease,  but  an  increase  in  the  bulk  of  certain 
muscles,  associated  with  a  change  in  their  consistence  and 
diminution  of  power,  and  due  to  an  overgrowth  of  the 
interstitial  connective  tissue,  and  subsequent  deposition 
of  fat,  is  observed  in  one  variety  of  the  progressive  mus- 
cular dystrophies  (pseudo-hypertrophic  muscular  paraly- 
sis). Muscular  hypertrophy,  both  the  true  and  false 
type,  occurs  in  Thomsen's  disease,  and  in  .the  healthy 
leg,  in  some  old  cases  of  poliomyelitis,  as  a  result  of  in- 
creased activity,  and  in  rare  cases  of  infantile  cerebral 
hemiplegia  with  athetosis  and  without. 

Altered  Electrical  Irritability  of  Nerves  and  Muscles — 
Reaction  of  Degeneration. — In  health  the  muscles  and 
motor  nerves  are  excitable  by  galvanism  and  faradism. 
Either  current,  when  applied  to  a  motor  nerve  ^  (indirect 
stimulation),  is  capable  of  producing  a  contraction  in 
the  muscle  or  muscles  supplied  by  this  nerve.  The  faradic 
current  causes  a  contraction  which  continues  during  its 
application,  but,  if  the  distinct  shocks  of  which  it  con- 
sists are  passed  through  the  nerve  at  short  intervals,  each 
stimulus  gives  rise  to  a  contraction  of  momentary  duration. 
A  galvanic  current  of  moderate  intensity  applied  to  the 
nerve  gives  rise  to  a  muscular  contraction  only  when  the 
circuit  is  made  or  broken — that  is,  when  the  current  is 
passed  or  stopped — or  when  a  sudden  change  is  made  in 
the  current  strength.  A  slight  diminution  in  the  irrita- 
bility of  the  nerve  to  both  faradic  and  galvanic  currents 

^  The  point  on  the  surface  at  which  a  motor  nerve  passes  to  its 
muscle  is  called  a  "  motor-point."  It  is  customary,  in  electro-diag- 
nosis to  obtain  contractions  by  stimulating  motor-points.  These  points 
are  given  in  most  text-books  on  general  medicine. 


SYMPTOMATOLOGY    OF   NERVOUS   DISEASES.       I9I 

is  observed  in  diseases  of  the  nervous  system  which  im- 
pair the  nutrition  of  either  the  upper  or  the  lower  motor 
segment  ;  considerable  diminution  or  complete  loss  of 
irritability  to  the  strongest  currents  is  observed  only  in 
disease  of  the  lower  segment  (degeneration  of  the  nerve- 
fibres  from  any  cause). 

Either  faradic  or  galvanic  current,  when  applied  to  a 
muscle  without  the  intervention  of  a  motor  nerve  (direct 
stimulation),  can  be  made  to  produce  a  contraction  of  this 
muscle.  The  muscle  possesses  two  irritable  structures, 
which  it  is  convenient  to  think  of  as  being  physiologically 
distinct  :  (i)  the  intra-muscular  termination  of  the  motor 
nerve-fibres  with  their  motorial  end-plates,  and  (2)  the 
muscular  fibres  themselves.  In  health  both  these  struc- 
tures may  be  excited  by  either  current,  but  it  is  probable 
that  it  is  mainly  by  the  action  of  these  currents  on  the 
motorial  end-plates  that  the  contractions  are  produced. 
When  these  end-plates  undergo  degeneration,  as  they  do 
in  consequence  of  degeneration  of  the  motor  nerve-fibres 
or  spinal  ganglion- cells  with  which  they  are  connected, 
and  the  motor  nerve  is  no  longer  excitable  by  faradism 
(vide  supra),  the  muscle  also  loses  its  faradic  irritability, 
because  faradism  is  incapable  of  stimulating  the  muscular 
fibres  themselves  when  these  have  suffered  in  their  nu- 
trition. But  the  galvanic  current,  notwithstanding  the  ex- 
istence of  nutritive  changes  in  the  muscle-fibres  and  from 
degeneration  of  the  nerve-fibres  and  motor  nerve-endings, 
is  still  capable  of  exciting  a  muscular  contraction,  by 
directly  stimulating  the  muscular  fibres.  The  contraction, 
however,  which  is  obtained  under  these  circumstances 
differs  from  that  which  is  obtained  in  health  in  several 
respects.  First,  it  occurs  more  readily  for  a  time  than 
the  contraction  of  health — that  is,  the  muscle  responds 
to  a  feebler  galvanic  current.  Secondly,  the  contraction 
is   not   the  quick,    sharp,   and   complete   contraction   of 


192  DISEASES   OF   THE   NERVOUS   SYSTEM. 

health,  but  is  '  tardy,  wave-like,  and  often  imperfect. 
Thirdly,  theref  is  a  change  in  the  readiness  of  response 
at  the  two  poles.  Under  normal  conditions  a  contraction 
occurs  more  readily  at  the  negative  pole  when  the  circuit 
is  closed  (kathodal  closure  contraction,  KCC),  than  at 
the  positive  pole  when  the  circuit  is  closed  (anodal 
closure  contraction,  ACC), — that  is,  KCC  >  ACC,  and 
with  a  current  of  sufficient  strength  to  produce  both 
ACC  and  KCC  the  latter  is  always  more  vigorous  than 
the  former.  Under  the  conditions  of  disease  of  which 
we  are  speaking  (complete  degeneration  of  the  lower 
motor  segment),  the  anodal  closure  contraction  either 
occurs  with  a  weaker  current  than  the  kathodal  closure 
contraction,  or  both  contractions  occur  with  equal  readi- 
ness—that is,  ACC  >  KCC,  or  ACC  =  KCC.  These 
different  changes  in  the  contractility  of  the  muscles — loss 
of  faradic  irritability,  temporary  increase  of  galvanic  irri- 
tability, with  changed  polar  reactions  and  sluggish  re- 
sponses— constitute  what  is  known  as  the  reaction  of 
degeneration,  which  may  be  conveniently  expressed  by 
the  symbol  RD.  The  RD  is  so  called  because  it  is  evi- 
dence of  a  degenerative  change  in  the  motor  nerve-fibres, 
which,  when  stimulated,  no  longer  react  to  either  current 
(vide  supra). 

We  have  here  described  what  may  be  called  the  com- 
plete or  typical  form  of  RD — the  form  which  is  observed 
in  the  severer  varieties  of  lesions  in  the  lower  segment  of 
the  motor  path,  acute  degenerative  or  inflammatory  pro- 
cesses in  the  nuclei  of  the  motor  nerve-cells  anywhere  in 
the  spinal  cord,  medulla,  pons,  or  crura  cerebri,  or  in  the 
motor  nerves  which  spring  from  these  cells.  Other  forms 
of  RD  exist,  however,  presenting  innumerable  differences 
in  the  degree  and  character  of  the  changes  in  electrical 
excitability.     Of  these,  there  are  two  forms  or  types  of 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.       I93 

RD  that  require  mention.  The  first  of  these  is  observed 
in  chronic  forms  of  degenerative  disease  of  the  lower 
segment  of  the  motor  path,  in  which  the  nutrition  of  the 
nerve-fibres  and  muscle-fibres  is  gradually  more  and  more 
impaired.  The  nerve-fibres  and  their  motorial  end-plates 
suffer  slowly  in  nearly  equal  degree,  and  there  is  conse- 
quently a  gradual  loss  to  faradism  and  to  galvanism  in 
both  nerve  and  muscle.  This  form  of  RD  differs  from 
the  complete  form,  in  that  at  no  period  of  the  degenera- 
tive process  is  the  irritability  of  the  nerve-fibres  lost  while 
that  of  the  muscle-fibres  is  preserved.  There  is  conse- 
quently no  time  when  the  muscles  show  an  increased 
irritability  to  galvanism  and  loss  of  irritability  to  faradism. 
The  other  phenomena  of  the  complete  form  are,  however, 
present  ;  there  is  the  characteristic  sluggish  response  to 
galvanism,  and,  generally,  the  alteration  in  polar  reaction. 
The  other  variety  of  degenerative  reaction  that  remains 
to  be  mentioned  is  termed  the  "  mixed  form."  It  is 
characterized  by  the  presence  of  slight  or  marked  changes 
in  the  irritability  of  the  muscles^  while  the  nerve  either 
reacts  normally  or  shows  only  slight  diminution  in  irrita- 
bility to  both  currents.  The  changes  in  the  muscle  vary 
considerably  in  different  cases.  Usually  there  is  increased 
or  diminished  galvanic  excitability,  changed  polar  reaction, 
and  sluggish  contraction.  The  galvanic  irritability  may 
be  nearly  normal,  however,  and  the  altered  polar  reactions 
and  tardy  contraction  may  not  be  very  pronounced.  The 
mixed  form  of  RD  is  observed  in  cases  where  some  mus- 
cle-fibres are  degenerated  and  others  in  the  same  muscle 
are  normal  or  nearly  normal,  this  condition  of  the  muscle- 
fibres  being  dependent  on  a  corresponding  mixture  of 
normal  and  degenerated  nerve-fibres  in  the  nerve.  Clini- 
cally it  is  observed  in  peripheral  paralyses,  in  progressive 

muscular  atrophy,  acute  and  subacute  poliomyelitis,  etc. 
13 


194         DISEASES   OF   THE   NERVOUS   SYSTEM. 

It  is  Important  to  note  the  fact  that  the  slow,  sluggish 
contractions  which  are  observed  in  RD  constitute  its 
most  important  and  characteristic  feature.  They  are 
present  even  in  the  slightest  grades  of  RD,  in  cases 
where  the  irritability  of  the  nerves  to  both  currents  is 
retained,  where  the  faradic  irritability  of  the  muscles  is 
only  slightly  diminished,  and  where  the  polar  reactions 
are  normal  or  only  slightly  modified. 

The  development  and  course  of  the  electrical  changes 
which  constitute  the  RD  vary  according  to  the  severity 
and  chronicity  of  the  morbid  processes  on  which  they 
depend.  In  cases  where  the  lesion  is  very  severe  and 
acute  in  its  development  (acute  neuritis,  acute  poliomye- 
litis, severe  nerve  injuries),  there  is  an  early  ^  and  rapid 
fall  in  the  irritability  of  the  nerve,  both  to  faradism  and 
galvanism  ;  in  the  course  of  two  or  three  weeks  the  irri- 
tability of  the  nerve  becomes  extinct.  In  the  muscle 
there  is  a  fall  in  faradic  irritability  which  corresponds  in 
time  and  extent  (being  due  to  the  nerve-endings)  with 
that  observed  in  the  nerve.  The  galvanic  irritability  ot 
the  muscles  may  remain  unchanged  for  several  days  after 
the  onset  of  the  lesion,  or  may  fall  slightly.  Then  oceans 
a  considerable  increase  in  irritability,  which  reaches  its 
height  in  about  a  month,  and  is  followed  by  a  gradual 
decline,  until,  after  the  lapse  of  a  year,  or,  in  some  in- 
stances, two  years,  no  reaction  can  be  obtained  with  a 
current  that  can  be  borne.^  In  such  a  case  there  is  no 
recovery  of  electrical  irritability  or  of  power  of  voluntary 
contraction.     In    somewhat   less  severe    cases    of   acute 

^  This  fall  usually  begins  about  the  middle  of  the  first  week,  some- 
times not  until  its  end. 

^  When  galvanic  irritability  of  the  muscle  is  extinct  to  ordinary 
modes  of  stimulation,  the  insertion  of  a  needle  into  the  muscle  as  one 
pole  of  the  battery  may  elicit  a  local  contraction. 


SYMPTOMATOLOGY   OF  NERVOUS   DISEASES.       195 

onset  the  condition  of  electrical  irritability  may  be  the 
same  as  that  just  described  during  the  early  months. 
Then,  after  a  period  varying  from  six  months  to  a  year, 
there  is  a  gradual  return  of  faradic  irritability  in  the  mus- 
cle and  afterwards  in  the  nerve.  In  chronic  lesions  of 
great  severity  (progressive  muscular  atrophy)  the  loss  of 
irritability  to  both  currents  in  muscle  and  nerve  is  very 
gradually  lost,  the  galvanic  irritability  of  the  muscle  en- 
during the  longest,  but  becoming  extinct  after  the  lapse 
of  a  few  or  several  years. 

In  lesions  of  acute  and  subacute  development,  but  of 
moderate  severity,  the  fall  in  nerve  irritability  does  not 
differ  greatly  in  rapidity  of  progress  or  degree  from  that 
observed  in  the  severest  forms.  Muscle  irritability  to 
faradism  begins  to  sink  in  the  course  of  a  week,  and  is 
lost  in  from  three  to  five  weeks.  For  a  week  or  ten  days 
there  may  also  be  a  fall  in  galvanic  excitability  corre- 
sponding to  that  for  faradism.  Then  occurs  a  rise  in 
galvanic  irritability  which  reaches  its  maximum  in  a  month 
or  six  weeks.  Very  soon  (six  weeks  to  three  months) 
there  is  a  reappearance  of  irritability  in  the  nerve,  and  in 
consequence  of  this  (the  intramuscular  nerve-endings 
sharing  in  the  nutritive  changes  in  the  nerve  trunk)  a 
reappearance,  in  slight  degree,  of  the  faradic  irritability 
of  the  muscle.  About  the  same  time  there  is  a  slight 
recovery  of  power.  The  excessive  galvanic  irritability 
may  continue  a  considerable  length  of  time  (three  or  five 
months)  before  returning  to  the  normal,  which  it  does 
gradually. 

In  lesions  of  slight  severity  there  is  frequently  a  slight 
rise  in  nerve  irritability.  This  may  last  several  weeks, 
and  be  followed  by  an  inconsiderable  fall  in  irritability, 
lasting  a  few  weeks  or  months.  Power  of  voluntary  con- 
traction is  -^iever  entirely  lost,  and  the  loss  which  occurs 


196         DISEASES   OF   THE   NERVOUS   SYSTEM. 


WEEKS 

1 

3 

•0 

do 

JO 

/oo 

! 

—1 
0 

/" 

"^»^_ 

-Jbi? »"  'Hal 

*"'*"*^'»^ 

• 

"■--, 

iL.W 

Li 
> 
OH 
UJ 

-z. 

■^^ 

-— 

--UfiTibiA,.., 

Line 

POWER 

NO  ^E 

IN  0  NT 

^0N£ 

DAYS 


\S 


30 


ro 


too 


-I 
o 

3 
Si 


nVSinK 


•■««;, 


'••^..- 


X 


.^' 


...-• 


UJ 
> 

Of 


^•X 


..•bAtiupi. 


POWER 


NONE 


NONE 


SklC-tiT 


KiDKMkBas 


FMi^ 


fONSi  0 


£:f\ABl-£ 


B 


FIG.    69. 

Fig.  A  shows  type  of  electrical  reactions  in  a  case  of  severe  and  permanent 
damage  to  a  nerve.  The  broken  lines  cf — 1^  in  this  and  the  follow- 
ing chart  show  the  state  of  galvanic  irritability.  The  broken  lines  ■■■■■■■■■■■£ 
show  the  state  of  faradic  irritability.  The  broken  curves  in  the  upper  half  o' 
each  chart  show  the  state  of  electrical  irritability  in  the  ?nuscle  :  the  dotted  lines 
in  the  lower  half  of  each  chart  show  the  state  of  electrical  irritability  in  the 
nerve.   The  horizontal  dotted  line  represents  the  normal  degree  of  irritability. 

Fig.  B  shows  type  of  electrical  reaction  in  a  case  of  slight  damage  to  a  nerve. 


SYMPTOMATOLOGY    OF   NERVOUS   DISEASES.      197 

is  recovered  from  in  from  three  to  six  weeks.  The  irrita- 
bility of  the  muscle  to  faradism  corresponds,  in  general, 
to  that  of  the  nerve,  but  there  is  seldom  increased  faradic 
irritability  even  when  this  occurs  in  the  nerve.  The  gal- 
vanic excitability  has  the  same  character  as  in  lesions  of 
moderate  severity,  but  the  increase  is  less  and  of  shorter 
duration. 

Since  the  extent  of  the  changes  in  nerve  and  muscle 
irritability  varies,  in  general,  with  the  severity  of  the 
degenerative  process  in  the  nerve,  we  have  in  the  RD  a 
valuable  aid  in  prognosis,  for  the  severity  of  the  case  and 
its  duration  (in  the  case  of  acute  lesions)  are  proportional 
to  the  loss  of  nerve  irritability.  If  there  is  complete  loss 
of  nerve  irritability,  and  greatly  increased  galvano- 
muscular  excitability,  with  sluggish  contractions,  etc.,  the 
degenerative  process  is  one  of  severity.  The  question 
then  arises  whether  or  not  regeneration  can  take  place 
within  the  nerve — that  is,  whether  or  not  there  will  be 
recovery  of  trophic  innervation,  return  of  power,  etc. 
The  possibility  of  some  recovery  is  not  gone  until  there  is 
complete  loss  of  irritability  to  both  currents  in  the  muscle, 
but  if  there  is  no  return  of  faradic  irritability  in  the 
muscles  at  the  end  of  a  year,  and  their  atrophy  has  been 
rapid  and  great,  only  slight  improvement,  at  best,  will 
occur.  If  the  lesion  is  an  acute  one,  and  the  muscles 
have  lost  their  faradic  irritability  after  the  lapse  of  a  week 
or  ten  days,  considerable  atrophy  will  certainly  follow, 
and  the  loss  of  motor  power  will  be  of  long  duration. 
If  the  faradic  loss  does  not  occur  until  two  or  three 
weeks  have  passed,  there  will  be  less  atrophy  and  earlier 
recovery,  but  the  paralysis  will  last  many  months.  If 
there  is  only  slight  loss  of  faradic  irritability,  or  no  loss 
whatever,  recovery  will  begin  in  the  course  of  a  few  weeks 
or  months. 


198  DISEASES   OF  THE  NERVOUS   SYSTEM. 

The  presence  of  RD,  as  already  stated,  indicates  dis- 
ease of  the  lower  segment  of  the  motor  path.  The  more 
important  clinical  conditions  in  which  it  is  observed  are 
poliomyelitis,  progressive  (spinal)  muscular  atrophy,  amyo- 
trophic lateral  sclerosis,  lesions  of  the  ganglion-cells  of 
the  anterior  horns  from  hemorrhage,  tumor,  syringo- 
myelia, etc.,  bulbar  paralysis,  injuries  of  the  peripheral 
nerves,  neuritis  of  all  kinds  (rheumatic  neuritis,  multiple 
neuritis,  toxic  paralyses,  and  paralyses  after  infectious  dis- 
eases). The  absence  of  RD  does  not  exclude  the  possi- 
bility of  a  slight  affection  of  the  anterior  horns  or  motor 
nerves.  It  may  be  absent  in  very  slight  peripheral  par- 
alyses from  injury.  On  the  other  hand,  RD  may  be 
present,  in  slight  degree,  in  cases  of  lead  poisoning  and 
slight  injury  to  a  nerve  in  muscles  that  show  no  appreci- 
able loss  of  power. 

Dmiinished  Irritability  of  nerve  and  muscle  to  both 
currents,  without  RD,  is  due  to  slight  changes  in  the 
peripheral  nerves,  which  may  or  may  not  depend  on  cor- 
responding changes  in  the  motor  ganglion-cells.  In  the 
case  of  lesions  in  the  upper  segment  of  the  motor  path 
(cerebral  paralysis — pyramidal  tract  lesions)  the  electrical 
changes  are  due  to  the  nutritive  alterations  produced  in 
the  motor  nerve-cells  by  the  irritative  influence  of  de- 
scending degeneration  in  the  pyramidal  tract. 

The  clinical  conditions  in  which  simple  diminution  of 
irritability  without  qualitative  change  is  observed,  are  as 
follows  : 

(i)  Cerebral  paralyses;  diminished  irritability  in  par- 
alyzed muscles  in  the  course  of  three  or  four  months, 
usually  preceded  by  a  rise  in  irritability. 

(2)  Spinal-cord  diseases  ;  bulbar  paralysis,  amyotrophic 
lateral  sclerosis  ;  sometimes  difficult  to  distinguish  from  the 
slighter  RD  which  occurs  in  some  of  these  conditions. 


SYMPTOMATOLOGY   OF  NERVOUS   DISEASES.      1 99 

(3)  Peripheral  nerve  disease  ;  after  slight  injuries, 
after  recovery  from  RD,  in  multiple  neuritis  and  in 
arsenical  paralysis. 

(4)  Muscular  conditions  ;  atrophy  from  disuse,  arthri- 
tic atrophy,  progressive  myopathic  atrophies  (muscular 
dystrophies). 

3.  Increased  Irritability  of  nerve  and  muscle  to 
both  currents,  without  qualitative  changes,  is  frequently 
observed  in  the  early  period  of  hemiplegia  when  irritative 
phenomena  are  present,  in  the  early  stage  of  acute  and 
subacute  myelitis,  in  the  early  stage  of  progressive  mus- 
cular atrophy  (the  increase  in  irritability  in  these  cases  is 
usually  very  great),  and  in  the  first  days  of  slight  neuritis. 
An  increase  has  also  been  observed  in  some  cases  of 
hemichorea,  tetany,  locomotor  ataxia  (pre-ataxic  stage), 
and  dementia  paralytica.  A  peculiar  variety  of  increased 
muscular  irritability  to  both  currents  is  that  which  occurs 
in  myotonia  congenita  (Thomsen's  disease),  and  is  hence 
called  the  myotonic  reaction.  The  myotonic  reaction 
consists  in  increased  faradic  contractility,  with  prolonged 
contraction  after  the  current  ceases,  and  in  excessive 
galvanic  irritability  when  the  circuit  is  closed  (ACC  and 
KCC),  with  exceedingly  sluggish,  lasting,  and  wavy  con- 
tractions.    The  nerve  excitability  is  normal. 

Vaso-Motor  Symptoms  are  of  frequent  occurrence 
in  the  course  of  both  organic  and  nutritional  disease  of 
the  nervous  system,  but  the  diagnostic  indications  fur- 
nished by  them  are  of  comparatively  little  importance 
and  will  be  only  briefly  mentioned  here. 

The  disturbances  which  are  the  expression  of  disor- 
dered vaso-motor  function  manifest  themselves  clinically 
as  local  or  general  changes  in  color  and  temperature,  or 
by  alterations  in  secretion,  or  by  the  presence  of  oedema. 
In  general,  all  these  changes  are  most  marked  in  acute 


200         DISEASES   OF   THE   NERVOUS   SYSTEM. 

lesions  of  an  irritative  character.  Local  changes  in  color 
and  temperature  are  observed  in  many  cases  of  cerebral, 
spinal,  and  peripheral  disease.  In  hemiplegia  there  is 
often  an  increase  of  J  degree  F.  in  the  temperature  of 
the  paralyzed  limb,  and  this  may  be  accompanied  by  dis- 
tinct redness  of  the  skin.  In  other  cases  there  is  a  fall 
in  the  surface  temperature  of  the  limbs  ;  they  become  pale 
and  livid.  A  slight  degree  of  oedema  is  frequently  ob- 
served in  the  paralyzed  extremity,  and  occasionally  there 
is  a  marked  local  increase  in  perspiration.  Any  or  all  of 
these  changes  may  be  produced  by  disease  of  the  cortex 
or  of  the  vaso-motor  path  from  it  to  the  posterior  limb  of 
the  internal  capsule. 

In  spinal-cord  disease  slight  vaso-motor  disturbances 
are  very  common,  and  more  marked  changes  are  always 
present  in  inflammatory  processes,  whatever  may  be  the 
position  of  the  disease.  At  first  the  changes  are  those 
produced  by  vaso-motor  dilatation  (redness,  increase 
of  temperature,  sometimes  sweating)  ;  later,  there  is 
depression  in  the  temperature  of  the  limbs  involved, 
which  become  livid,  often  extremely  so,  at  the  ex- 
tremities. OEdema  is  not  uncommon  in  the  early- 
stages  of  acute  processes,  but  may  also  accompany 
disease  of  exceedingly  slow  development  (for  example, 
syringomyelia). 

In  diseases  of  the  peripheral  nerves  vaso-motor  dis- 
turbance is  of  frequent  occurrence  and  has  the  same 
character  as  spinal-cord  disease.  Very  slight  neuritis  is 
capable  of  producing  very  marked  changes  in  the  tem- 
perature of  a  part  for  a  considerable  period  of  time. 

It  is  thus  seen  that  no  deductions  as  to  the  position  of 
the  lesion  can  be  made  from  the  existence  of  vaso- 
motor symptoms  ;  these  must  be  made  from  the  associat- 
ed conditions  (motor  paralysis,  sensory  symptoms,  muscu- 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      201 

lar  atrophy,  etc.)  which  are  commonly  present,  and  from 
the  general  distribution  of  the  phenomena. 

Peripheral  vaso-motor  disturbance  is  not  at  all  infre- 
quent in  hysteria  and  allied  conditions,  and  is  often  most 
marked  in  its  manifestations.  The  distinction  of  vaso- 
motor symptoms  of  functional  origin  from  those  that  de- 
pend on  organic  disease,  is  usually  simple,  and  is  based 
on  the  mutability,  temporary  duration,  and  dependence 
on  emotional  disturbance,  which  is  observed  in  the  for- 
mer. The  extent  to  which  the  vaso-motor  apparatus  is 
under  the  influence  of  psychical  processes  is  illustrated 
by  the  fact  that,  in  rare  instances,  local  hyperaemia  and 
even  vesication  have  been  produced  by  verbal  suggestion 
in  subjects,  usually  hysterical,  in  the  hypnotic  state. 

The  "  iache  chebrale^''  or  better,  dermographism,  in 
which  slight  cutaneous  irritation  is  followed  by  distinct 
local  congestion  of  the  skin  of  considerable  duration,  is 
a  vaso-motor  disturbance  dependent  on  loss  of  tone  in 
the  smaller  vessels  from  defective  innervation  of  the 
local  ganglia  in  their  walls.  It  is  not  diagnostic  of  men- 
ingitis, as  has  been  supposed,  but  is  observed  in  many 
different  conditions  in  which  the  general  nervous  system 
suffers  in  its  nutrition. 

Mental  Symptoms. — Loss  of  Consciousness  is  one  of 
the  most  significant  and  frequent  symptoms  of  organic 
disease  of  the  brain,  but  since  it  is  also  a  symptom  of 
many  conditions  that  do  not  depend  on  structural  disease, 
but  on  nutritional  disturbance  of  the  cortex  (functional 
disease),  its  exact  significance  depends  largely  on  its 
associations.  The  expression  "  loss  of  consciousness,"  as 
employed  in  medicine,  refers  to  loss  of  the  external  mani- 
festations of  mental  activity,  not  to  the  loss  on  the  part  of 
the  patient  of  purely  subjective  consciousness,  though  the 
two  may  coincide.  Considerable  variations  in  the  degree 
of  unconsciousness  occur.     In  cases  where  it  is  possible 


202         DISEASES    OF   THE   NERVOUS   SYSTEM. 

to  rouse  temporarily  the  patient  from  his  sleep,  the  loss 
of  consciousness  is  regarded  as  partial,  and  is  termed 
"stupor."  When  the  loss  is  complete  and  the  patient 
cannot  be  roused  by  any  ordinary  stimulus  (voice,  rub- 
bing, slapping),  the  condition  is  termed  "  coma "  if  it 
endures  longer  than  a  few  minutes.  In  coma  there  is 
partial  or  complete  loss  of  control  over  the  sphincters, 
superficial  reflex  action  is  generally  lessened  or  lost,  the 
muscles  are  relaxed,  and  there  may  be  loss  of  the  deep 
reflexes.  The  pupils  are  usually  dilated  and  immobile ; 
sometimes  they  are  contracted  (generally  in  toxic  states). 
The  pulse  is  often  slow  and  irregular  in  force  and  fre- 
quency ;  sometimes  it  is  rapid  and  feeble.  Respiration 
is  diminished  in  frequency  and  force.  The  relaxation  of 
the  palate  permits  it  to  vibrate  with  the  air-current  and 
gives  rise  to  stertorous  breathing.  Frequently  the  res- 
piration is  irregular,  and  sometimes  it  presents  the 
rhythmical  changes  in  depth  known  as  "  Cheyne-Stokes 
respiration." 

In  stupor,  on  the  other  hand,  the  reflexes,  both  super- 
ficial and  deep,  are  retained,  the  pharyngeal  reflex  may 
be  excited,  and  the  pupils  react  to  light,  but  there  is 
usually  some  loss  of  sphincter  control. 

Loss  of  consciousness  may  be  produced  by  almost  any 
one  of  the  pathological  processes  to  which  the  brain 
is  subject.  In  every  case  the  impairment  of  conscious- 
ness probably  depends  on  interference  with  the  highest 
functions  of  the  cortex,  and  such  interference  may  be  due 
either  to  disease  of  the  cortex  itself,  or  to  the  inhibitory 
action  of  lesions  elsewhere  in  the  brain. 

Chronic  processes  impair  consciousness  either  through 
the  involvement  of  a  considerable  area  of  the  brain  cortex, 
or  by  increasing  greatly  or  rapidly  the  intracranial  pres- 
sure.    Lesions  of  sudden  onset  (hemorrhage  or  soften- 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      203 

ing)  on  the  contrary,  may  cause  loss  of  consciousness 
in  whatever  region  of  the  brain  they  may  be  situated, 
probably  by  their  irritative  inhibitory  effect  on  the  cortex. 
When  the  loss  of  consciousness  is  suddenly  produced,  as 
it  usually  is  in  acute  lesions,  it  is  termed  "  apoplexy." 
Cerebral  hemorrhage  ^  is  by  far  the  most  frequent  cause 
of  apoplexy,  and  on  this  account  the  word  is  frequently 
used  synonymously  with  "  hemorrhage  into  the  brain  " 
Apoplexy  may  also  result  from  the  arrest  of  blood  supply 
which  leads  to  cerebral  softening,  and  may  be  caused  by 
embolism  or  thrombosis  of  a  cerebral  artery.  Sometimes 
it  results  from  simple  concussion  (often  slight)  of  the 
brain,  and  in  rare  cases  it  can  be  ascribed,  on  reasonable 
grounds,  to  congestion.  In  old  persons  apoplexy  occa- 
sionally occurs  without  the  existence  of  any  cerebral 
changes  to  which  it  can  be  attributed.  In  dementia 
paralytica  also,  apoplectic  attacks  occur  which  cannot 
be  satisfactorily  accounted  for.  Temporary  loss  of  con- 
sciousness, of  sudden  onset,  occurs  in  epilepsy  and  con- 
stitutes an  important  feature  of  the  paroxysms.  Of 
the  causes  outside  the  nervous  system  that  may  give  rise 
to  loss  of  consciousness  those  that  depend,  like  uraemia, 
diabetes,  and  cholaemia,  on  the  production  of  toxic  sub- 
stances in  the  organism  (auto-intoxication),  and  those 
that  depend  on  the  introduction  of  poisons  from  without 
(alcohol,  opium,  chloral),  are  the  most  important.  The 
loss  of  consciousness  of  cardiac  syncope  in  anaemia 
depends  on  a  temporary  deficiency  in  the  cerebral  cir- 
culation, and  should  be  classed  with  the  functional 
varieties  of  such  loss. 

The  diagnosis  of  the  cause  of  coma  is  often  a  matter 
of  the  greatest  moment  on  account  of  its  bearing  on  prog- 

^  Depressed  fracture  of  the  skull  is  also  a  frequent  cause  of  loss  of 
consciousness,  but  only  pathological  causes  are  considered  here. 


204         DISEASES   OF   THE   NERVOUS   SYSTEM. 

nosis  and  treatment,  but  is  often  attended  with  considera- 
ble difficulty.  It  frequently  happens  that  a  patient  is 
brought  to  a  hospital  in  coma,  and  that  the  medical 
attendant  is,  for  the  time  at  least,  without  any  knowledge 
of  the  previous  history  of  the  case.  The  correct  diagno- 
sis in  such  a  case  rests  on  its  objective  features,  arid 
every  case  of  coma  requires  an  exceedingly  careful 
examination.  Even  then  it  is  frequently  impossible. 
The  points  of  distinction  between  the  different  organic 
diseases  (hemorrhage,  thrombosis,  embolism,)  which  may 
give  rise  to  coma  are  described  in  Chapter  V.,  but  the 
main  differences  between  coma  of  organic  cerebral  origin 
and  the  loss  of  consciousness  that  is  due  to  functional 
disease  of  the  brain,  or  to  toxic  influences,  will  be  briefly 
mentioned.  In  every  instance  focal  symptoms  of  brain 
disease  are  to  be  looked  for.  Hemiplegia  may  be  detect- 
ed during  coma,  if  there  is  some  restlessness,  as  the  move- 
ments are  most  marked  or  confined  to  one  side,  but  if  the 
coma  be  very  deep,  evidence  of  paralysis  may  be  entirely 
wanting.  The  presence  of  hemiplegia  must  then  be  infer- 
red from  other  indications,  and  of  these  the  most  important 
are  the  condition  of  the  reflexes,  the  unequal  move- 
ments of  the  superior  intercostals  on  the  two  sides,  and 
the  presence  of  Babinski's  sign.  The  unilateral  loss  of 
the  abdominal,  plantar,  or  tendon  reflex  (knee-jerk)  makes 
the  existence  of  a  one-sided  cerebral  lesion  probable,  and 
this  probability  is  considerably  increased  if  two  or  more 
of  these  reflexes  are  absent.  On  the  other  hand,  if  no 
distinct  abnormality  in  the  skin  or  deep  reflexes  can  be 
detected,  and  there  are  no  decided  indications  of  hemi- 
plegia or  other  focal  symptom,  it  is  improbable  that  there 
is  a  cerebral  lesion.  Conjugate  deviation  of  the  eyes  is 
usually  evidence  of  a  unilateral  organic  cerebral  lesion, 
the  deviation  being  usually  to  the  side  of  the  lesion.  If 
there  is  no  evidence  of  an  organic  lesion  the  loss  of  con- 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES,      205 

sciousness  is  probably  due  to  functional  disease  of  the 
brain,  or  to  some  toxic  condition, — as  alcoholic,  diabetic, 
or  uraemic  intoxication.  Of  the  functional  states  that 
cause  coma  the  chief  are  epilepsy  and  hysteria. 

Post- Epileptic  Stupor  is  usually  of  short  duration  (one 
to  two  hours  at  most,  even  after  a  series  of  seizures);  the 
patient  can  be  easily  roused  ;  one-sided  symptoms  are 
absent,  except  in  hemiplegic  (old)  epilepsy  ;  the  temper- 
ature is  normal  or  slightly  elevated,  and  the  loss  of 
consciousness  is  followed  by  temporary  headache  and 
often  by  a  confused  state  of  mind.  An  epileptic  also 
usually  bears  physical  stigma  of  his  disease — bromic 
acne,  bruises,  etc. 

Hysterical  Coma  occurs  in  patients  of  the  sex  and  age 
that  suggest  hysteria,  is  generally  preceded  by  other  symp- 
toms of  hysteria  (especially  convulsion  or  headache),  and 
is  characterized,  even  in  cases  of  apparently  profound 
unconsciousness,  by  the  preservation  of  the  power  of 
swallowing.  There  are  no  distinctive  objective  symptoms, 
but  varying  rigidity  of  the  muscles  and  twitching  of  the 
eyelids  are  very  frequently  observed.  If  headache  has 
been  present  it  ceases  when  the  coma  comes  on. 

Urcemic  Coma  may  closely  resemble  apoplexy  from  an 
acute  cerebral  lesion.  In  both  conditions  there  may  be 
albuminuria  and  convulsions.  The  absence  of  albumen 
in  the  urine  is  strongly  against  uraemia,  but  not  absolutely 
so;  its  presence  has  not  much  significance,  except  in  per- 
sons under  thirty-five  years  of  age.  Repeated  convulsions 
occurring  at  short  intervals  favor  uraemia  ;  single  or  few 
convulsive  seizures  make  it  improbable.  The  convulsions 
of  uraemia  may  have  a  local  commencement,  and  may 
remain  local  (unilateral)  ;  usually  they  are  general.  The 
presence  of  neuro-retinitis  of  the  albuminuric  type 
strongly  suggests,  but  does  not  prove,  that  the  coma 
depends  on  uraemia,  and  its  absence  does  not  exclude  the 


206         DISEASES   OF   THE   NERVOUS   SYSTEM. 

ursemic  oriofin  of  the  coma.  Continuous  subnormal  tem- 
perature  favors  uraemia.  If  there  is  a  history  of  sudden 
complete  blindness  before  the  coma  this  makes  its  uraemia 
origin  practically  certain.  The  pupils  are  usually  dilated 
in  uraemia  coma. 

Alcoholic  Coma  may  be  exceedingly  difficult  to  distin- 
guish from  the  coma  of  hemorrhage  or  softening.  Its 
duration  is  short,  there  are  no  unilateral  symptoms,  and 
there  is  usually  evidence  of  drinking.  The  presence  of 
alcohol  in  the  breath  is  of  course  no  proof  that  the  coma 
is  due  to  alcohol.  It  may  be  necessary  to  wait  a  few 
hours  before  coming  to  a  positive  conclusion. 

Diabetic  Coma  may  be  preceded  by  other  cerebral  symp- 
toms, especially  headache,  and  sometimes  convulsions. 
The  diagnosis  is  based  on  the  detection  of  glucose  and 
acetone  in  the  urine,  both  of  which  are  probably  present 
in  all  cases  of  diabetic  coma.  Acetone  is,  however, 
present  in  many  conditions,  especially  gastro-intestinal 
disorders,  other  than  diabetes.  The  breath  in  diabetic 
coma  often  smells  of  acetone. 

Delirium. — The  word  delirium  is  employed  to  ex- 
press very  different  ideas.  As  used  here  it  is  intended  to 
designate  illogical  and  incoherent  mental  processes,  as 
expressed  in  word  or  act.  The  perversion  of  mental  ac- 
tivity that  occurs  in  delirium  is  distinguished  from  the 
similar  alteration  that  constitutes  insanity  by  its  acute 
course  and  temporary  duration,  and  by  its  dependence  on 
pyrexia,  toxaemia,  or  organic  disease  of  the  brain.  In 
what  is  termed  "  quiet  "  delirium  there  are  sensory  images 
without  corresponding  sensory  impressions — "  hallucina- 
tions,"— or  actual  peripheral  impressions  give  rise  to  false 
sensory  images — "illusions."  There  are  false  ideas  or 
delusions,  the  nature  of  which  is  frequently  determined 
by  the  character  of  the  hallucinations  or  illusions.  The 
patient  generally  talks  incoherently  in   a  low   tone,  and 


SYMPTOMATOLOGY   OF   NERVOUS    DISEASES.     20/ 

often  this  muttering  speech  is  almost  continuous.  He 
lies  quietly  in  bed  or  exhibits  only  slight  restlessness.  In 
"  active  "  delirium,  on  the  contrary,  the  patient  is  restless 
and  may  attempt  to  leave  his  bed.  He  attempts  to  act 
according  to  his  delusions,  and  in  these  attempts  he  may 
commit  acts  which  threaten  his  life  or  that  of  his  attend- 
ant. The  delusions  of  delirium  change  rapidly  in  char- 
acter and  never  present  the  systemized  and  elaborate 
character  of  those  observed  in  some  forms  of  insanity. 
There  is  rarely  much  emotional  depression. 

Delirium  is  much  more  often  dependent  on  pyrexia, 
toxaemia,  etc.,  than  upon  organic  disease  of  the  nervous 
system.  The  cerebral  processes  on  which  it  depends 
most  often  are  meningitis,  tumor,  extensive  softening,  and 
cerebritis.  The  occurrence  of  delirium  in  the  course  of 
spinal-cord  and  peripheral-nerve  disease  (myelitis,  multi- 
ple neuritis)  depends  on  the  pyrexia  which  accompanies 
these  processes,  and  not  on  their  situation  or  nature. 
The  character  of  the  delirium  gives  no  clue  in  determin- 
ing whether  it  is  due  to  pyrexia,  its  most  frequent  cause, 
or  to  organic  disease  of  the  brain.  If,  in  a  given  case, 
delirium  is  the  only  symptom  referable  to  the  nervous 
system,  it  can  be  attributed  to  organic  disease  of  the 
brain  only  if  the  body  temperature  is  below  loi  °  F.,  be- 
cause the  existence  of  a  temperature  greater  than  this 
makes  it  probable  that  the  delirium  is  referable  to  the 
pyrexia.  In  persons  who  habitually  use  alcohol  in 
excess,  in  those  who  are  in  debilitated  health,  and  in  the 
aged,  a  slighter  degree  of  fever  may  give  rise  to  delirium, 
and  this  must  be  borne  in  mind  in  forming  an  opinion  of 
its  significance.  But  the  coexistence  of  delirium  and  a 
temperature  above  loi  °  is  indicative  of  the  non-organic 
origin  of  the  delirium  only  in  cases  where  there  are  no 
symptoms  suggestive  of  encephalic  disease,  and  such 
symptoms  should  be  sought  for  with  the  greatest  care 


208         DISEASES   OF   THE   NERVOUS   SYSTEM. 

before  a  conclusion  is  reached.  The  occurrence  of 
muscular  rigidity,  convulsions,  diplopia,  or  strabismus,  or 
of  repeated  vomiting,  should  excite  grave  suspicion  of 
organic  mischief.  The  coexistence  of  optic  neuritis 
makes  organic  disease  practically  certain,  for,  although 
optic  neuritis  sometimes  occurs  after  acute  infectious  dis- 
eases, it  does  not  in  these  cases  make  its  appearance 
until  after  the  height  of  the  disease  has  been  passed. 
The  association  of  delirium  and  headache  is  exceedingly 
important.  If  the  headache  is  severe  it  should  excite 
suspicion  of  organic  disease.  The  headache  of  fever 
usually  lessens  or  ceases  when  delirium  is  developed. 
Hence  the  persistence  of  slight  headache  is  an  equivocal 
symptom. 

Simple  Mental  Deterioration  is  of  frequent  occurrence 
both  in  cases  of  nutritional  and  organic  brain  disease. 
It  is  manifested  chiefly  by  defective  memory — amnesia. 
Memory  is  subserved,  in  all  probability,  by  the  same 
physical  elements  that  subserve  intellectual  processes 
generally,  and  of  these  the  structures  that  make  up  the 
cerebral  cortex  and  bring  into  association  its  constituent 
cell-elements  are  the  most  important.  Loss  of  memory 
may  result  from  any  condition  of  disease  which  impairs 
the  nutrition  of  the  brain  generally  or  that  of  the  cortex. 
It  is  observed  after  acute  infectious  diseases,  after  severe 
mental  shock  (often  such  as  occurs  from  the  fright 
experienced  when  an  injury  is  received),  in  hysteria,  in 
epilepsy,  and  in  neurasthenia.  It  results  also  from  vari- 
ous organic  processes,  particularly  from  those  that  involve 
the  cortex  or  the  subjacent  white  matter — meningitis, 
hemorrhage,  softening,  new  growths,  and  degenerative 
processes  (dementia  paralytica,  dementia  senilis).  In- 
ability to  concentrate  the  attention  is  often  associated 
with  amnesia,  and  may  be  its  cause,  the  loss  of  memory 
being  apparent  rather  than  real. 


,SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.     209 

Defects  in  the  Moral  Sense  are  very  apt  to  be  associ- 
ated with  mental  failure.  Often  the  change  is  slight  and 
difficult  of  estimation  by  the  physician.  In  given  cases 
the  degree  of  defect  can  be  measured  only  by  comparison 
with  the  previous  moral  status  of  the  individual.  It  is 
exceedingly  important  to  take  into  account  the  signifi- 
cance of  slight  defects  in  the  moral  sense  of  which  the 
patient  is  unconscious,  and  which  contrast  with  the 
patient's  previous  sense  of  propriety.  Such  defects  are 
always  of  serious  import.  They  are  often  the  first  indi- 
cations of  dementia  paralytica,  making  their  appearance 
before  the  unsystematized  and  characteristic  delusions  of 
this  disease.  A  rude  disregard  of  the  comfort  or  interests 
of  others  in  one  who  has  been  habitually  thoughtful  in 
these  respects,  or  the  telling  of  unnecessary  and  usually 
blundering  falsehoods  by  one  who  has  always  been 
strictly  truthful,  should  in  adults  always  excite  some 
suspicion  of  degenerative  brain  disease.  This  is  par- 
ticularly true  if  the  moral  defects  are  associated  with 
conspicuous  loss  of  memory  or  defective  power  of  atten- 
tion. The  refusal  to  swallow  food  when  there  is  no 
pharyngeal  paralysis  is  usually  an  indication  of  a  consid- 
erable degree  of  mental  failure.  Indecent  exposure  of 
the  body,  or  the  passage  of  urine  and  faeces  in  the  bed 
when  there  is  no  sphincteric  paralysis,  are  evidences, 
except  in  children,  of  considerable  mental  or  moral 
change.  The  passage  of  urine  and  faeces  in  the  bed, 
under  these  conditions,  is  frequent  in  some  forms  of  or- 
ganic cerebral  disease — softening,  dementia  paralytica,  etc. 

Disturbances  of  Speech. — Disturbances  of  speech* 

^  The  word  speech  is  here  used  in  its  broadest  sense — that  is,  to 

denote  the    ability   of    one  individual   to   communicate   thought   to 

another  by  means  of  symbols,  and  to  recognize  such  symbols  when 

made  by  others. 
14 


2IO        DISEASES   OF  THE   NERVOUS  SYSTEM. 

are  of  frequent  occurrence  in  brain  disease,  and  often  give 
indications  as  to  the  position  of  the  disease  which  gives 
rise  to  them.  Hence  they  are  of  considerable  diagnostic 
importance  and  deserve  careful  study.  The  symptoms 
of  speech  affection  are,  however,  numerous  and  highly 
intricate  in  their  relations,  and  their  study  is  rendered 
difficult  by  the  circumstance  that  accurate  information  as 
to  the  effects  of  local  lesions  in  producing  these  symptoms 
is  still  scanty.  Often,  too,  the  same  facts  are  susceptible 
of  different  interpretations. 

Two  distinct  mechanisms  exist  for  the  expression  of 
articulate  speech.  One  of  these,  situated  in  the  cortex 
of  the  brain,  subserves  the  arrangement  of  the  various 
elements  which  enter  into  speech.  This  may  be  termed 
the  higher  speech  mechanism.  The  other,  consisting  of 
nerve-cells  in  the  medulla  and  pons,  is  related  to  the  form 
and  not  to  the  arrangement  of  the  speech  elements — 
that  is,  it  is  simply  concerned  with  the  articulation  of 
words.  This  is  the  lower  speech  mechanism.  It  is 
brought  into  use  by  stimuli  which  descend  to  it  from 
the  higher  mechanism.  Disease  of  the  lower  speech 
mechanism  gives  rise  to  defects  or  loss  of  articulation. 
Disease  of  the  higher  speech  mechanism  gives  rise  to 
defects  in  the  use  and  arrangement  of  words. 

Defects  of  Articulation  (dysarthria,  anarthria)  may  result 
from  any  lesion  involving  the  lower  speech  mechanism 
(nuclei  of  hypoglossal  and  facial  nerves)  or  the  peripheral 
paths  from  it  (that  is,  the  lower  segment  of  the  motor 
path  to  the  muscles  concerned  in  speech).  Whenever 
there  is  considerable  defect  in  articulation  there  is  appre- 
ciable paralysis  of  the  muscles  concerned  in  articulate 
speech.  The  defect  may  be  due  to  unilateral  or  bilateral 
palsy.  Defective  articulation  may  arise  also  from  disease 
in  the  upper  segment  of  the  motor  path,  either  in  the 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      211 

cortex  or  in  the  path  from  it.  When  the  disease  is  unila- 
teral, the  speech  defect  is  usually  transient,  because  com- 
pensation takes  place  from  the  other  hemisphere  ;  but  if 
the  disease  is  bilateral — that  is,  involves  the  structures 
concerned  in  articulation  in  both  hemispheres, — the  defect 
is  permanent. 

The  changes  in  articulation  that  depend  on  disease  of 
the  lower  segment  of  the  motor  path  vary  according 
to  the  muscles  that  are  involved  in  the  palsy.  Palsy  of 
the  tongue  causes  imperfect  articulation  of  the  Unguals  / 
and  t.  Paralysis  of  the  lips  causes  their  imperfect  ap- 
proximation and  consequent  defect  in  the  pronunciation 
of  labial  consonants.  P^  b,  and  n  are  replaced  by  f  and 
V.  Paralysis  of  the  palate  gives  the  voice  a  nasal  and 
monotonous  quality.  It  also  causes  imperfect  pronuncia- 
tion of  the  consonants  /  and  b  ("  explosive  "  labials), 
because  non-closure  of  the  nares  hinders  the  compression 
of  air  within  the  mouth  necessary  for  their  production. 
Separation  of  syllables,  changes  in  rhythm,  and  sudden 
explosive  utterance  of  words  in  what  is  termed  "  scanning 
speech"  (also  "staccato"  speech),  is  a  form  of  disturb- 
ance frequently  observed  in  multiple  sclerosis,  of  which  it 
is  rather  characteristic,  and  occasionally  in  chorea  and  in 
affections  causing  imperfect  transmission  of  impulses 
from  partial  damage  to  nerve-roots.  "  Confluent  "  artic- 
ulation is  one  of  the  manifestations  of  slighter  disease 
of  the  bulbar  mechanism,  and  consists  in  the  running 
together  of  terminal  consonants  and  syllables  with  those 
that  follow. 

Speech  Defects  Dependent  on  Disease  of  the  Cerebral  Hemi- 
sphere and  expressed,  not  as  defects  in  articulation,  but  as 
errors  in  the  arrangement  or  nature  of  the  speech  ele- 
ments, are  designated  by  the  word  aphasia.  Cerebral 
processes  of  speech  are  either  motor  or  sensory  in  char- 


212         DISEASES   OF   THE   NERVOUS   SYSTEM. 

acter,  and  the  leading  forms  of  speech  defects,  motor 
aphasia  and  sensory  aphasia^  are  due  to  derangement  of 
the  corresponding  processes  of  speech.  The  motor 
speech  processes  are  those  by  which  language  is  uttered. 
They  are  effected  in  the  posterior  part  of  the  third  frontal 
convolution,  and  possibly  also  in  the  neighboring  part  of 
the  anterior  central  convolution.  In  the  lower  part  of  the 
anterior  central  convolution  of  either  side  is  the  centre  for 
the  muscles  concerned  in  articulation^  which  is  interfered 
with  by  the  bilateral  involvement  of  these  cortical  centres, 
as  already  mentioned,  and  to  some  extent  by  their  uni- 
lateral involvement.  The  motor  speech  centre  (Broca's 
centre),  in  which  the  arrangements  for  the  expression 
of  word  processes  is  effected,  must  be  carefully  dis- 
tinguished from  the  articulatory  centre  just  mentioned. 
The  two  are  adjacent  and  perhaps  some  structures  are 
common  to  both,  but-articulation  may  be  impaired  with- 
out impairment  of  the  higher  motor  processes,  and  the 
latter  may  be  impaired  without  any  defect  in  the  power 
of  articulation,  though  frequently  both  are  impaired 
together.  From  the  centre  for  the  movement  of  the 
lips  and  tongue,  fibres  pass  through  the  internal  capsule 
to  the  lower  mechanism  of  articulation. 

A  lesion  destroying  the  left  motor  speech  centre  usually 
gives  rise  to  total  loss  of  voluntary  speech  (motor 
aphasia).  The  loss  is  of  voluntary  speech  only,  because 
emotional  and  automatic  speech  is  subserved  by  both 
hemispheres,  and  is  continued  by  the  speech  centres  of 
the  right  hemispheres  when  those  of  the  left  are  damaged. 
In  persons  who  are  right-handed  the  speech  centre  for 
voluntary  speech  is  in  the  left  hemisphere,  the  corre- 
sponding centre  on  the  right  side  being  related  only  to 
involuntary  and  automatic  utterance,  although  it  is  capable 
of  being  educated  to  supplement  the  action  of  the  struc- 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      213 

tures  on  the  left  side.  In  those  who  are  left-handed, 
although  they  may  use  the  right  hand  for  writing,  vol- 
untary speech  is  subserved  by  the  centre  in  the  right 
hemisphere. 

Not  only  may  voluntary  speech  be  lost  in  consequence 
of  extensive  destruction  of  the  motor  speech  centre,  but 
there  may  be  impairment  of  expression  by  means  of 
gestures.  The  patient  may  for  a  time  make  with  his 
head  the  sign  of  negation  when  he  wishes  to  express 
assent.  Very  soon  there  is  some  recovery  of  the  ability 
to  say  simple  words  like  "yes"  and  "no."  These  words 
may  be  employed  in  two  ways — as  propositions,  to  express 
the  ideas  of  assent  and  dissent  (propositional  use),  and 
as  interjections,  for  the  expression  of  emotion,  and  they 
may  be  regained  and  employed  as  interjections  before 
they  are  again  acquired  as  propositions.  Many  other 
words  possess  these  two  forms  of  use,  and  the  proposi- 
tional use  is  always  regained  the  later.  Thus  many 
patients  can  swear  or  sing  songs  who  could  not  deliber- 
ately and  propositionally  make  use  of  the  words  of  an 
oath  or  of  a  song.  In  some  cases  a  considerable  degree 
of  speech  loss  persists  for  a  long  period  of  time.  In  the 
majority  of  cases  there  is  slow  recovery  of  speech  after 
the  lapse  of  a  few  months,  so  that  eventually  recovery  of 
language  occurs.  When  the  lesion  in  the  speech  region 
is  destructive  in  character,  this  ultimate  recovery  of 
language  is  unquestionably  due  to  compensation  through 
education  of  the  right  hemisphere  (speech  centre)  for 
higher  processes  than  it  originally  subserved  (voluntary 
speech).  The  extent  to  which  this  supplemental  action 
of  the  undamaged  speech  area  is  possible  varies  greatly 
even  in  adults.  In  children  it  occurs  to  an  astonishing 
extent.  It  is  exceedingly  rare  to  see  motor  aphasia  in  a 
child  in  consequence  of  disease  in  the  left  hemisphere. 


214        r»I>EASE<   '^'T  THE  XERVOrS  SYSTEM, 


sT^^i  rep:>ii  i>  i.bo'ira  by  tiie  ^ct  iktt  a 
a  tbis 

ofificniL    h  M»-4esa«clH«  IcBOBs  of  tke  left 
of  iMKd  odML  saw  Reofciy  of 


SYMPTOMATOLOGY    OF   NERVOUS   DISEASES.      21 5 

middle  of  the  ascending  frontal  convolution  of  either 
side.  From  these  centres  the  motor  impulses  are  con- 
ducted by  the  pyramidal  tracts  to  the  cord,  and,  through 
it  and  the  peripheral  path  to  the  writing  hand.  It  is 
important  to  note  that  the  ability  to  write  does  not 
depend  on  paralysis  of  the  movements  of  the  arm  and 
hand,  for,  even  when  these  movements  are  perfect,  a 
lesion  in  the  motor  speech  centre  causes  agraphia. 
Agraphia  is  also  caused  by  a  small  lesion  involving  the 
subcortical  tract  from  the  speech  centre  to  the  hand 
centre.  The  loss  of  the  power  of  writing,  like  motor 
aphasia,  may  be  complete  or  partial.  When  the  loss  is 
partial,  the  errors  in  writing  are  similar  in  character  to 
those  which  occur  in  speaking,  and  frequently  they  are 
greater.  In  these  cases  the  power  of  copying  is  pre- 
served. 

Motor  aphasia  is  not  always  the  consequence  of  disease 
of  the  cortex.  It  may  follow  interruption  of  the  conduct- 
ing tract  to  the  hand  centre  of  the  same  side,  which  lies 
just  beneath  the  cortex,  or  a  lesion  in  the  internal 
capsule.  If  the  lesion  is  in  the  internal  capsule  the  loss 
of  speech  is  transient ;  if  beneath  the  cortex  it  may  be 
permanent.  No  disturbance  of  intellect  is  necessarily 
associated  with  motor  aphasia. 

Motor  aphasia  may  be  produced  by  any  pathological 
process  which  involves  the  speech  region  or  the  subjacent 
white  matter.  It  is  most  frequently  produced  by  cerebral 
softening.  The  motor  speech  area  lies  within  the  province 
of  the  first  branch  of  the  middle  cerebral  artery  (see 
Fig.  57),  and  hence  must  suffer  if  this  is  occluded  by 
embolism  or  thrombosis.  Aphasia  from  hemorrhage, 
though  less  frequent  than  that  from  softening,  is  also  fre- 
quent. Tumor  is  not  an  infrequent  cause.  In  children 
tubercular  meningitis  is  frequently  operative  in  producing 


2l6         DISEASES   OF   THE   NERVOUS    SYSTEM. 

motor  aphasia,  for  the  irritation  of  meningitis  seems  com- 
petent to  inhibit  the  speech  centre  as  it  does  the  motor 
centres. 

Sensory  speech  processes  subserve  the  reception  and 
revival  of  language.  It  is  chiefly  through  the  senses  of 
hearing  and  sight  that  these  processes  are  brought  into 
activity,  and  there  is  consequently  a  close  connection 
between  these  senses  and  the  disturbances  of  speech 
which  depend  on  the  arrangement  of  the  sensory  pro- 
cesses, auditory  and  visual,  of  speech.  Such  disturbances 
of  speech  are  designated  sensory  aphasia^  the  leading 
varieties  of  which  are  word-deafness  and  word-blindness. 

In  Word- Deaf 7iess  words  that  are  spoken  by  another 
are  not  understood.  This  does  not  depend  on  deafness 
in  the  ordinary  sense ;  the  patient  hears  the  spoken 
words,  but  they  are  meaningless  to  him.  Words  of  his 
own  language  sound  strange  ;  there  is  failure  to  associate 
these  words  with  the  ideas  they  represent.  Word-deafness 
depends  on  disease  of  the  posterior  half  of  the  first  tem- 
poral convolution,  usually  of  the  left  side.  This  is,  there- 
fore, the  situation  of  the  structures  that  subserve  the 
auditory  perception  of  words,  but  it  is  also  the  situation 
of  the  auditory  centre  itself.  Whether  the  two  centres, 
the  auditory  perceptive  centre  and  the  auditory  centre, 
are  identical  it  is  impossible  to  say.  They  are  at  present 
indistinguishable.  When  this  region  of  the  cortex  is  dis- 
eased there  is  usually,  in  addition  to  word-deafness, 
transient  deafness  in  the  ear  opposite  the  lesion. 

When  word-deafness  exists  there  is  always  distinct  de- 
rangement of  speech.  This  is  because  the  revival  of  the 
memory  of  words  in  the  mind,  before  their  arrangement 
in  the  motor  speech  centre,  previous  to  utterance,  occurs 
mainly  in  the  auditory  perceptive  centre  of  the  cortex. 
Without  this  ability  to  revive  past  auditory  impressions 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.     217 

the  patient's  memory  for  words  depends  on  his  faculty  for 
reviving  the  motor  processes  for  words  which  have  left 
behind  changes  in  the  cortical  cells  (residual  states) 
which  facilitate  this  revival — that  is,  he  has  to  fall  back 
on  what  may  be  called  his  motor  memory.  This  is  im- 
perfect, and  errors  in  the  form  and  use  of  words  occur 
even  when  the  word-deafness  is  only  partial. 

Word-deafness  is  rarely  absolute,  because  the  auditory 
perceptive  centre  is  habitually  aided  in  the  automatic 
revival  of  words  by  corresponding  centres  in  the  right 
hemisphere.  Considerable  recovery  of  the  ability  to  under- 
stand spoken  words  and  of  the  voluntary  revival  of  words 
usually  occurs  in  the  course  of  time,  and  this  is  due  to 
the  education  of  the  latent  powers  of  the  right-sided  centre. 

In  word-deafness  the  patient  is  not  conscious  of  the 
errors  of  speech  which  he  makes.  In  this  respect  there  is 
a  striking  contrast  with  motor  aphasia,  in  which  the  patient 
not  only  appreciates  his  errors  but  tries  to  correct  them. 

Word- Blindness  is  the  inability  to  comprehend  the 
written  symbols  of  language.  There  is  usually  no  loss 
of  sight  ;  the  patient  sees  letters  and  words,  but  he  fails 
to  recall  to  mind  the  ideas  they  represent.  The  position 
of  the  lesion  that  gives  rise  to  word-blindness  cannot  at 
present  be  definitely  located.  The  symptom  may  be 
produced  by  a  lesion  in  the  inferior  parietal  lobule,  and 
perhaps  also  by  lesions  involving  the  angular  gyrus  or 
the  occipital  lobe  of  the  left  side.  In  word-blindness 
there  is  usually  some  error  in  the  use  and  form  of  words, 
but  in  some  cases  this  is  very  slight.  Word-blindness 
and  word-deafness  often  coexist.  Usually  the  power  of 
speaking  is  retained. 

Mind-Blindness  ("  soul-blindness  *')  is  a  rare  condition 
in  which,  without  mental  defect,  there  is  entire  loss  of 
visual  memory   of  every  kind      The  patient  no  longer 


2l8         DISEASES   OF   THE   NERVOUS   SYSTEM. 

recognizes  familiar  faces  or  objects.  There  is  also  loss 
of  recognition  of  visual  word  symbols — that  is,  the  loss 
includes  word-blindness,  which  may  be  regarded  as  par- 
tial mind-blindness.  The  lesion  in  cases  of  mind-blind- 
ness is  probably  in  the  posterior  part  of  the  parietal 
lobes  and  in  the  occipital  lobes,  anterior  to  the  half  vision 
centres  (p.  50).  Probably  permanent  mind-blindness 
is  due  to  bilateral  involvement  of  these  areas.  Some- 
times hemianopsia  is  associated  with  mind-blindness. 

Mind- Deaf tiess  is  a  rare  condition  in  which,  without 
mental  defect,  there  is  loss  of  auditory  memory.  This 
symptom  is  especially  striking  in  musicians,  who  may 
lose  the  faculty  of  appreciating  music  or  following 
melodies,  or  of  playing  or  following  notes. 

The  word  Apraxia  is  used  as  a  general  term  to  desig- 
nate an  inability  to  recognize  the  meaning  or  use  of  an 
object.  Hence  there  are  as  many  varieties  of  apraxia  as 
there  are  modes  of  special  sensation.  Both  mind-blind- 
ness and  mind-deafness  are  varieties  of  apraxia. 

Alexia^  or  inability  to  read  unde r standingly ^  is  of 
course  an  essential  feature  of  word-blindness.  It  is 
important,  however,  to  recognize  the  fact  that  alexia  may- 
result  from  a  pure  motor  aphasia.  In  many  persons, 
particularly  those  who  are  imperfectly  educated,  motor 
speech  processes  are  essential  to  the  comprehension  of 
written  speech  symbols  ;  a  kind  of  internal  speech  goes 
on  while  these  persons  are  reading,  the  external  evidence 
of  which  is  the  movement  of  the  lips  which  is  often  seen 
in  these  persons.  When  these  persons  are  deprived  of 
their  motor  word-processes  by  disease,  alexia  results. 
The  alexia  gradually  lessens,  however,  because  some 
motor  word  processes  are  regained,  and  serve  to  rein- 
force the  visual  centre.  When  the  alexia  is  due  to  word- 
blindness    the    inability     to    comprehend    visual    word 


SYMPTOMATOLOGY    OF   NERVOUS   DISEASES.      219 

symbols  is  absolute,  and  the  motor  speech  processes  are 
generally  unimpaired. 

Dyslexia  is  a  term  applied  to  a  rare  symptom  consist- 
ing in  a  peculiar  condition  of  mental  fatigue  from  read- 
ing, which  makes  its  appearance  a  few  minutes  after  the 
patient  begins  to  read,  and  makes  it  impossible  to  read 
more  than  a  few  words  consecutively.  There  is  no 
motor  speech  disturbance.  This  condition  is  not  asso- 
ciated with  any  visual  defect,  and  is  unaccompanied  by 
ocular  pain.  It  is  thought  to  depend  on  a  subcortical 
lesion  beneath  the  angular  gyrus. 

Amnesic  Aphasia,  or  difficulty  in  voluntarily  recalling 
words,  particularly  those  which,  like  nouns,  are  special 
in  character,  may  result  either  from  partial  word-deafness 
or  from  pure  motor  aphasia.  It  is  claimed  that  in  cases 
where  amnesic  aphasia  is  the  only  form  of  speech  defect 
from  the  beginning  it  constitutes  a  distinct  variety  of 
aphasia,  and  depends  on  a  distinct  pathological  condi- 
tion. This  condition  is  supposed  to  be  a  lesion  which 
interrupts  the  conducting  path  between  the  motor  and 
auditory  centres,  and  thus  prevents  that  action  of  the 
auditory  on  the  motor  speech  centre  which  is  essential 
to  the  perfect  revival  of  motor  word-processes.  For  this 
reason  it  has  been  termed,  somewhat  unfortunately, 
"  conduction  aphasia  "  (''  Leitungs  Aphasie  ").  It  can- 
not be  said  that  the  evidence  on  the  strength  of  which 
amnesic  aphasia  is  considered  a  distinct  variety  of 
aphasia  is  as  satisfactory  as  could  be  desired. 

Speech  disturbances  are  not  always  due  to  organic 
disease  of  the  brain.  They  occur  not  infrequently  as  an 
expression  of  functional  derangement  of  the  cerebral 
centres.  Thus,  transient  motor  aphasia  often  occurs  after 
right-sided  convulsions  from  any  cause,  probably  from 
the  exhaustion  of  the  motor  speech  centre  which  results 


220         DISEASES   OF   THE   NERVOUS   SYSTEM. 

from  the  discharge  of  nerve  force.  In  migraine  slight 
motor  or  sensory  aphasia  is  not  very  uncommon  during 
the  attacks,  especially  in  right-handed  persons,  when 
there  is  some  sensory  disturbance  (tingling,  numbness) 
in  the  right  limbs,  particularly  the  arm.  Partial  motor 
aphasia  occasionally  occurs  during  emotion  or  excite- 
ment, m  persons  (women)  of  hysterical  character.  In 
severe  cases  of  typhoid  fever  motor  aphasia,  usually 
transient,  has  many  times  been  noted.  In  some  of  these 
cases  it  was  unquestionably  of  organic  origin  ;  in  others 
it  has  occurred  under  conditions  which  make  probable 
its  dependence  on  defective  cortical  nutrition  from  the 
morbid  blood  state. 

Congenital  aphasia,  motor  or  sensory,  is  exceedingly 
rare,  and  when  it  exists  probably  depends  on  traumatic 
meningeal  hemorrhage  during  labor. 

The  ability  of  an  aphasic  patient  to  make  a  will  may 
constitute  an  important  practical  question.  In  order  that 
a  valid  will  may  be  made,  it  is  necessary  that  the  testator 
should  be  able  (i)  to  understand  the  proposition  that  is 
put  before  him,  and  (2)  that  he  should  be  able  to  ex- 
press assent  or  dissent  in  an  unmistakable  manner.  If 
there  is  word-deafness  it  is  impossible  to  say  with  cer- 
tainty that  the  patient  understands  what  is  said  to  him, 
and  hence  a  valid  will  cannot  be  made  if  what  is  put 
before  the  testator  is  spoken.  If,  however,  the  patient 
understands  written  words,  and  propositions  are  com- 
municated in  writing  only,  word-deafness  is  no  obstacle 
to  the  making  of  a  will.  The  coexistence  of  word-deaf- 
ness and  word-blindness  of  course  destroys  all  testament- 
ary capacity.  Motor  aphasia,  even  absolute  in  degree,  does 
not  destroy  testamentary  capacity  if  spoken  words  are 
understood  and  if  the  testator  can  indicate  assent  and 
dissent  by  means  of  signs. 


SYMPTOMATOLOGY    OF   NERVOUS    DISEASES.      221 

General  Symptoms.^  Temperature. — Elevation  of 
temperature  is  of  frequent  occurrence  in  nervous  disease. 
The  fever  may  be  simply  an  associated  condition — that  is, 
the  morbid  process  in  the  nervous  system  and  the  eleva- 
tion of  temperature  are  referable  to  a  common  cau^. 
This  is  particularly  the  case  with  processes  that  are  due 
to  infection — for  example,  some  forms  of  multiple  neuri- 
tis, poliomyelitis,  cerebral  embolism,  etc.  In  some  con- 
ditions it  is  difficult  to  say  to  what  extent  the  fever  is 
due  to  the  general  condition  or  the  morbid  process  in 
the  nervous  system.  This  doubt  arises,  for  instance, 
when  tubercular  meningitis  and  general  tuberculosis 
occur  together.  The  fever  may  be  dependent  chiefly  on 
the  character  of  the  process  without  particular  reference 
to  its  situation  in  the  nervous  system.  Acute  inflamma- 
tory processes  in  any  position  are  attended  with  fever, 
which  is  generally  to  be  regarded  as  consecutive  to  the 
inflammation.  In  the  case  of  intracranial  disease  an 
important  peculiarity  is  frequently  observed  :  There 
may  be  only  slight  rise  of  temperature  or  even  no  rise 
of  temperature  in  the  course  of  inflammatory  processes 
of  considerable  or  great  severity.  This  is  true,  for  exam- 
ple, in  some  cases  of  meningitis.  This  peculiarity  prob- 
ably depends  on  the  inhibitory  influence  of  irritative 
processes  on  the  heat  centres  of  the  medulla.  It  is 
important  to  remember  that  the  absence  of  fever  or  its 
slight  degree  does  not  indicate  the  absence  of  inflamma- 
tion within  the  cranium. 

Sometimes  the  pyrexia  that  results  from  central  nervous 
disease  depends,  not  on  the  nature  of  the  pathological 
process,  but  upon  its  direct  action  on  the  heat  centres,  or 
the  apparatus  which  controls  them.  This  is  particularly 
the  case  with  acute  lesions  (hemorrhage,  softening)  in  the 
upper  part  of  the  cervical  cord,  medulla,  pons,  or  optic 


222         DISEASES   OF   THE   NERVOUS   SYSTEM. 

thalami.  In  these  cases  there  is  often  a  rapid  and  great 
rise  in  temperature — the  fever  may  rise  to  103°  or  to 
105°,  and  in  the  case  of  medullary  and  pontine  lesions 
even  higher  (io6°-io8°).  Death  usually  follows  such 
ah  elevation  of  temperature  within  a  short  time.  In 
some  cases  of  sunstroke  very  high  temperatures  are  seen 
(io8°-iio°),  and  there  is  often  a  great  premortal  rise  in 
cases  of  meningitis.  In  the  case  of  sunstroke  the  hy- 
perpyrexia does  not  necessarily  foreshadow  a  fatal 
termination. 

Sometimes  the  rise  of  temperature  is  the  secondary 
effect  of  nervous  disease,  particularly  disease  of  the 
brain.  Any  condition — for  example,  tetanus,  epilepsy — 
which  gives  rise  to  many  successive  attacks  of  convul- 
sions is  followed  by  a  rise,  often  considerable,  in  tempera- 
ture. This  is  due  apparently  to  the  excessive  muscular 
action,  aided  possibly  by  the  accumulated  and  retained 
products  of  extraordinary  tissue  destruction,  caused  by 
the  convulsions.  During  the  "  status  epilepticus  "  '  (p. 
576)  the  temperature  may  rise  to  io6°-io9°.  There  is 
not  uncommonly  a  post-mortem  rise  in  temperature  in 
status  of  epilepsy,  general  paresis,  uraemia,  and  in  many 
other  states  terminated  by  a  series  of  convulsions. 

A  subnormal  temperature  sometimes  occurs  in  brain 
disease,  rarely  in  disease  of  other  parts  ot  the  nervous 
system.  The  process  which  gives  rise  to  it  is  generally 
hemorrhage,  the  depression  of  temperature  occurring 
usually  at  its  onset.  If  the  extravasation  of  blood  be 
great,  the  temperature  may  fall  to  95°,  93°,  or  even  90° 
(rectal).  In  such  cases  there  are  the  usual  signs  of  col- 
lapse. A  slight  initial  fall  may  be  succeeded  by  a  rise  in 
temperature. 

Pulse. — Most  forms  of  organic  nervous  disease  have  no 

^  111  this  state  the  paroxysms  recur  at  short  intervals  for  a  consider- 
able time  (often  many  hours  or  days). 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.     223 

special  effect  on  the  rapidity,  force,  or  rhythm  of  the 
pulse.  Inflammatory  intracranial  disease  may  inhibit  the 
pulse  rate  even  when  there  is  a  considerable  elevation  of 
temperature,  and  it  is  not  uncommon  in  meningitis  to 
meet  with  a  temperature  of  103°  or  104°  and  a  pulse  rate 
which  is  normal  or  even  less  than  normal.  A  higher  tem- 
perature from  intracranial  disease  is  generally  associated 
with  a  soft  and  rapid  pulse.  Infrequency  of  the  pulse 
rate  (50-40-30  per  minute)  is  sometimes  observed  at  the 
onset  of  acute  lesions  (hemorrhage,  softening).  A  habit- 
ually rapid  pulse  rate  (90-120  per  minute),  without  fever, 
is  not  uncommon  in  neurasthenia  and  some  forms  of  hys- 
teria. Marked  irregularity  of  pulse  is  often  an  important 
early  sign  of  irritative  intracranial  disease,  such  as  tumor. 

Respiration  is  markedly  influenced  by  organic  disease 
of  the  nervous  system  chiefly  when  this  is  extensive 
(hemorrhage,  softening),  or  when  it  involves  the  parts  in 
the  neighborhood  of  the  respiratory  centre  in  the  medulla. 
In  such  cases  respiration  is  often  exceedingly  irregular, 
both  as  regards  rhythm  and  rate,  and  may  eventually 
cease  from  exhaustion  of  the  respiratory  centre.  Sud- 
den cessation  of  respiration  occurs  from  a  sudden  lesion 
(hemorrhage,  thrombosis,  embolism)  in  the  respiratory 
centre  of  one  side  or  both  sides,  and  may  occur  from  in- 
hibition of  this  centre  from  acute  lesions  adjacent  to  the 
centre.  When  the  lesion  is  external  to  but  near  the  re- 
spiratory centre,  the  depression  of  respiration  may  con- 
tinue many  hourSj  and  then  disappear  spontaneously. 
Irregularity  in  the  rhythm  and  force  of  the  respiratory 
movements  is  often  observed  in  inflammatory  cerebral 
lesions.  It  is  especially  frequent  in  acute  meningitis,  and 
is  so  common  and  so  decided  in  most  cases  of  tubercular 
meningitis  as  to  be  rather  characteristic  of  this  disease. 

The  paradoxical  respiratory  sign  (page  90)  is  to  be 
found  in  all  capsular  lesions  of  hemiplegia. 


224        DISEASES   OF   THE   NERVOUS   SYSTEM. 

Cheyne-Stokes  respiration  (peculiar  rhythmical  changes 
in  breathing,  characterized  chiefly  by  the  alternation  of 
periods  during  which  there  is  a  gradual  and  extreme  dim- 
inution in  the  force  and  frequency  of  the  respiration, 
with  periods  of  increasing  depth  of  breathing,  these 
periods  being  separated  by  a  variable  interval  of  time — 
5-40  seconds)  is  sometimes  observed  toward  the  close  of 
cerebral  diseases  (hemorrhage,  meningitis,  tumor,  and 
status  epilepticus).  The  patient  is  usually  comatose  and 
rarely  recovers  when  this  form  of  breathing  has  begun. 
Cheyne-Stokes  breathing  occurs  in  many  diseases  ex- 
ternal to  the  nervous  system  (heart  disease,  pneumonia, 
nephritis,  diphtheria,  etc.),  and  under  these  circum- 
stances is  of  less  grave  significance  than  when  due  to 
brain  disease.  Its  explanation  may  rest  upon  the  bi- 
lateral withdrawal  of  cerebral  inhibitory  influence-  upon 
the  medullary  centres. 

Mucus  accumulates  in  the  bronchi  and  trachea  in 
states  in  which  the  cerebral  functions  are  in  abeyance, 
for  example,  in  the  course  of  prolonged  coma.  The 
bronchial  and  tracheal  rales  which  result  must  not  be 
mistaken  for  bronchitis.  Passive  congestion  of  the  lungs 
and  hypostatic  pneumonia  are  of  common  occurrence 
under  the  same  circumstances,  and  constitute  a  frequent 
cause  of  death  in  central  nervous  disease. 

Of  the  symptoms  referable  to  the  Digestive  Organs^ 
Vomiting  is  by  far  the  most  important.  As  an  effect  of 
organic  nervous  disease  vomiting  is  chiefly  observed  in 
intracranial  disease,  although  it  is  not  uncommon  as  an 
effect  of  acute  processes  in  the  upper  cervical  cord,  and 
occurs  paroxysmally  in  some  chronic  general  diseases  of 
the  spinal  cord  (locomotor  ataxia). 

Vomiting  occurs  as  a  symptom  of  organic  disease  of  the 
brain  in  many  different  conditions — in  meningitis,  tumor, 
abscess,  and  not  infrequently  in  cerebral  hemorrhage — 


SYMPTOMATOLOGY   OF  NERVOUS  DISEASES.      22$ 

that  is,  in  irritative  conditions.  Sometimes  it  occurs  re- 
peatedly in  the  course  of  endarteritis  of  vessels  of  the 
base,  before  complete  obstruction  takes  place.  Generally 
speaking,  any  condition  giving  rise  to  considerable  in- 
crease in  intracranial  pressure  may  occasion  vomiting. 
The  situation  of  the  lesion  does  not  seem  to  exert  any 
important  influence  in  determining  the  symptom,  except- 
ing in  the  case  of  cerebellar  lesions,  which  are  particularly 
apt  to  give  rise  to  it. 

Vomiting  of  cerebral  origin  cannot  be  said  to  possess 
any  features  that  are  to  be  regarded  as  highly  distinctive. 
Still,  certain  characters,  chiefly  negative,  of  such  vomit- 
ing are  sufficiently  frequent  to  be  suggestive.  These  are  : 
(i)  The  rejection  of  food  soon  after  its  ingestion;  (2) 
the  absence  of  discomfort  after  eating  ;  (3)  the  absence 
of  nausea  ;  and  (4)  the  absence  of  other  gastric  symptoms. 
In  general  the  vomiting  of  functional  nervous  disease 
(hysteria)  possesses  the  same  negative  characteristics. 
Hence  it  is  that  the  diagnostic  significance  of  vomiting 
depends  mainly  on  its  associations.  The  organic  processes 
which  give  rise  to  vomiting  are  exceedingly  apt  to  cause 
persistent  headache,  or  optic  neuritis,  or  both.  The  as- 
sociation, therefore,  of  either  of  these  symptoms  and,  a 
fortiori^  of  both  of  them,  with  frequent  vomiting,  makes 
intracranial  disease  probable. 

The  vomiting  of  intracranial  disease  depends  on  an  in- 
creased excitability  of  the  gastric  centre  in  the  medulla. 
When  this  exaltation  of  excitability  is  great,  vomiting 
may  occur  spontaneously — that  is,  without  any  trace- 
able gastric  cause.  Before  this  high  degree  of  irritability 
is  reached,  slight  peripheral  causes,  such  as  dietetic  indis- 
cretion, may  cause  vomiting  more  readily  than  would 
be  the  case  in  the  absence  of  this  increased  irritability. 
Hence  it  is  easy  to  understand  the  vomiting  which  may 
be  the  first  indication  of  organic  disease.     Every  patient, 

»5 


226        DISEASES   OF   THE   NERVOUS   SYSTEM. 

and  particularly  every  child,  who  vomits  without  experi- 
encing the  indisposition  that  generally  attends  vomiting 
from  gastric  cause,  should  be  carefully  watched.  The 
vomiting  which  is  associated  with  vertigo  has  already 
been  mentioned. 

Constipation  usually  accompanies  cerebral  and  spinal- 
cord  diseases  which  are  attended  with  elevation  of  tem- 
perature, but  has  little  diagnostic  significance.  Obstinate 
constipation  is  almost  a  constant  symptom  of  destructive 
disease  of  the  cord  above  the  lumbar  enlargement. 

The  pathological  changes  that  occur  in  The  Urine  as 
the  result  of  nervous  disease  are  few,  and,  generally 
speaking,  of  little  help  in  diagnosis.  Transient  albumi- 
nuria and  glycosuria  are  occasionally  observed  in  disease 
of  various  parts  of  the  brain,  and  particularly  in  lesions 
of  the  medulla  and  pons.  Much  more  frequently  albumi- 
nuria is  associated  with  diseases  of  the  cerebral  vessels 
(endarteritis,  hemorrhage,  atheroma,  miliary  aneurisms) 
which  result  in  cerebral  hemorrhage  or  softening.  Other 
urinary  changes  (oxaluria,  excessive  or  insufficient  excre- 
tion of  uric  acid,  increase  in  indican,  etc.)  are  common  in 
nutritional  diseases  of  the  nervous  system,  as  neuras- 
thenia, some  forms  of  headache,  etc.  These  changes  are, 
as  yet,  not  sufficiently  understood  to  be  of  material  aid 
in  diagnosis,  but  it  is  likely  that  in  the  future  they  will 
prove  of  considerable  help  in  the  diagnosis  of  the  nature 
of  nutritional  diseases  of  the  nervous  system. 

Affections  of  the  Sphincters  of  the  Bladder  and  Anus  are 
of  frequent  occurrence  in  organic  disease  of  the  nervous 
system,  but  are  not  common  from  disease  of  the  pe- 
ripheral nerves  external  to  the  spinal  column.  Interrup- 
tion of  the  voluntary  path  (probably  the  pyramidal  tract) 
from  the  brain  cortex  to  the  reflex  centres  for  the  bladder 
and  rectum  in  the  lumbar  enlargement  of  the  cord  (lowest 
lumbar  and  sacral  segments)  results  in  the  loss  of  volun- 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.      22/ 


tary  control  of  the  functions 
of  these  viscera.  Their  ac- 
tion becomes  purely  reflex. 
As  soon  as  a  sufficient 
amount  of  urine  accumu- 
lates in  the  bladder,  the  vis- 
cus  is  emptied  by  the  reflex 
contraction  of  the  detrusor 
urinae  and  synchronous  re- 
laxation, also  reflex,  of  the 
sphincter  ;  when  faeces  ac- 
cumulate in  the  rectum  and 
irritate  its  mucous  mem- 
brane, they  are  expelled 
by  an  analogous  mechan- 
ism. The  incontinence  of 
urine  is  called  ''  intermit- 
tent "  or  "reflex  inconti- 
nence." It  is  important 
to  understand  that  there  is 
no  paralysis  of  the  sphinc- 
ters in  this  form  of  inconti- 
nence. The  proof  of  this  is 
(in  the  case  of  the  rectum) 
that  the  introduction  of  the 
finger  into  the  rectum  is 
followed,  after  slight  relaxa- 
tion, by  firm  and  tonic  con- 
traction of  the  sphincter. 
The  interruption  of  the  vol- 
untary path  which  results  in 
this  loss  of  cerebral  control 
may  result  from  different 
conditions  ;  generally  from 


FIG.  70. 


Diagram  illustrating  the  innervation 
of  the  bladder  and  the  effect  of  lesions 
in  various  parts  of  the  spinal  cord  upon 
the  function  of  micturition.  A  lesion, 
A,  which  interrupts  the  voluntary  path 
to  the  bladder  centre  in  the  sacral  cord, 
causes  incontinence  of  urine;  when  a 
sufficient  quantity  of  urine  accumulates 
in  the  bladder  there  occurs  a  reflex  con- 
traction of  the  detrusor  and  relaxation 
of  the  sphincter.  The  sensory  path 
from  the  cord  to  the  brain  being  unin- 
volved,  the  patient  is  conscious  of  the 
process,  but  cannot  exercise  voluntary 
control  over  it.  With  a  lesion,  B, 
which  involves  also  the  sensory  path, 
the  patient  is  unconscious  of  the  filling 
and  reflex  emptying  of  the  bladder.  A 
lesion,  C,  which  causes  destruction  of 
the  sacral  reflex  centre  for  the  bladder 
causes  continuous  dribbling  of  urine, 
and  not  its  automatic  expulsion  at  in- 
tervals. 


228         DISEASES   OF   THE   NERVOUS   SYSTEM. 

spinal-cord  disease  (myelitis  or  injury  above  the  lumbar 
enlargement,  lateral  sclerosis,  etc.).  In  reflex  inconti- 
nence there  is  usually  some  weakness  of  the  detrusor 
urinae  after  a  time.  Then  retention  occurs,  and  the  dis- 
tension of  the  bladder  leads  to  relaxation  of  the  sphinc- 
ter and  incontinence — "  overflow  incontinence."  When 
the  functions  of  the  brain  are  in  abeyance  (stupor,  coma) 
from  any  cause,  there  may  be  retention  of  urine  and  in- 
continence, but  the  incontinence  consists  in  these  cases 
of  the  dribbling  of  urine  from  a  full  bladder,  "  overflow 
incontinence,"  and  there  is  no  actual  weakness  of  the 
sphincter.  There  is  also  involuntary  passage  of  faeces 
in  these  cases. 

The  reflex  apparatus  for  expelling  the  contents  of  the 
bladder  and  rectum,  and  for  preventing  their  continuous 
evacuation  may  be  disordered  in  its  function  by  disease 
involving  the  rectal  and  vesical  centres  in  the  lumbar  en- 
largement, or  the  efferent  and  afferent  nerves  connected 
with  these  centres.  Most  frequently  the  disturbance  of 
function  depends  on  destructive  disease  of  the  lumbar 
centres.  In  this  condition  faeces  or  urine  are  passed  as 
soon  as  they  enter  the  rectum  or  bladder.  The  urine 
dribbles  away  continuously  ;  the  condition  of  the  rectal 
sphincter  can  be  determined  by  the  introduction  of  the 
finger,  which  shows  it  to  be  persistently  relaxed.  When 
there  is  partial  damage  to  the  lumbar  centres,  of  gradual 
development,  there  is  often  difficulty  in  exciting  the 
action  of  the  detrusor  (patient  "  cannot  start  his  urine  "), 
and  this  may  result  in  retention.  Damage  to  the  cauda 
equina  sometimes  produces  disturbances  like  those  that 
result  from  partial  disease  of  the  lumbar  centres  for  the 
bladder  and  rectum. 

Disorders  of  the  Sexual  Functions  are  of  frequent 
occurrence  in  nervous  diseases,  but  do  not  possess  much 
diagnostic  importance,  and  will  be  only  briefly  touched 


SYMPTOMATOLOGY   OF   NERVOUS   DISEASES.       229 

upon.  They  are  more  common  as  the  result  of  functional 
than  of  organic  disease.  The  sexual  act  is  largely  a  reflex 
act,  and  its  perfect  performance  depends  on  the  integrity 
of  a  reflex  arc  whose  centre  lies  in  the  sacral  cord  near 
that  for  the  bladder  and  rectum.  The  action  of  this 
centre  is,  however,  to  some  extent  under  cerebral  control, 
and  in  this,  as  in  other  respects,  the  sexual  reflex  re- 
sembles closely  the  skin  reflexes. 

Disease  of  the  sexual  centre  in  the  sacral  cord,  or  of 
the  nerves  leading  to  or  from  it,  causes  loss  of  sexual 
power,  as  shown  in  the  male  by  loss  of  erectile  and  ejac- 
ulatory  power.  Thus  the  sexual  reflex  is  lost  with  loss 
of  control  over  the  anal  and  vesical  sphincters,  when  the 
lumbo-sacral  cord  is  destroyed,  as  in  myelitis.  In  loco- 
motor ataxia  it  is  lost  from  disease  of  the  sensory  portion 
of  the  arc.  When  the  damage  is  partial  in  the  reflex  arc 
the  corresponding  loss  of  function  is  partial  only. 

Disease  which  cuts  off  the  controlling  path  from  the 
brain  to  the  reflex  sexual  centre  causes  over-action  of  this 
centre  with  resulting  priapism.  This  is  seen  in  dorsal 
myelitis,  compression  and  crush  of  the  cord,  etc.  In 
women  various  menstrual  disorders  may  accompany  or- 
ganic disease,  especially  cord  disease.  Periods  of  great 
sexual  excitement  occur  in  some  women  with  locomotor 
ataxia  (so-called  "  clitoris  crises  ").  A  great  variety  of 
sexual  disturbances,  including  increased  and  diminished 
sexual  desire,  spermatorrhoea,  and  priapism,  are  observed 
in  functional  disorders  (hysteria,  neurasthenia,  traumatic 
neuroses).  In  some  cases  of  hysteria  deep  pressure  over 
the  ovarian  region,  especially  the  left,  causes  severe  and 
characteristic  pain,  often  with  nausea  and  vomiting,  and 
perhaps  excites  an  hysterical  paroxysm. 


CHAPTER    III. 

THE    DIAGNOSIS    OF    THE    POSITION    OF    THE    LESION 

LOCALIZATION. 

It  is  convenient  to  think  of  all  morbid  processes  affect- 
ing the  nervous  system  as  divisible  into  two  great  groups 
— those  which  consist  of  changes  in  the  cell-elements,  that 
are  demonstrable  by  present  methods  of  investigation 
(organic  diseases),  and  those  that  consist  of  alterations  of 
variable  degree  in  the  nutrition  of  these  elements,  but 
are  unassociated  with  demonstrable  structural  changes 
(nutritional  or  "functional"  diseases).  These  two 
groups  merge  into  one  another  insensibly,  both  in  their 
pathological  and  clinical  characters,  but  for  practical 
purposes  their  separation  is  desirable,  and  the  general 
principles  on  which  the  clinical  distinction  of  organic 
and  functional  disease  is  based  are  elsewhere  presented 

(P-  556). 

This  distinction,  which  occasionally  constitutes  a 
problem  of  the  greatest  difficulty,  ordinarily  is  made  with 
ease,  and  having  been  made,  at  least  provisionally,  should 
be  followed  by  a  systematic  endeavor  to  obtain  more 
accurate  knowledge  of  the  morbid  process.  In  general, 
an  effort  should  be  made — first,  to  locate  as  accurately  as 
possible  the  seat  of  the  morbid  process  within  the 
nervous  system  (local  diagnosis) ;  and,  secondly,  to 
determine  the  pathological  nature  of  this  process  (patho- 
logical diagnosis). 

230 


DIAGNOSIS  OF   THE  POSITION  OF  THE  LESION.      23I 

In  the  case  of  organic  disease  on  the  nervous  system  it 
is  of  great  practical  importance  to  locate  accurately,  /.<?.,  to 
"  localize  "  the  lesion  (which  includes  an  estimate  of  its 
extent),  because  this  information  not  only  is  an  important 
guide  to  prognosis,  but  may  furnish  the  most  important 
indications  for  treatment/ 

Fortunately  the  data  now  at  command  enable  a  local 
diagnosis  to  be  made  with  precision  in  a  large  majority  of 
all  cases  of  organic  nervous  disease. 

In  the  case  of  functional  disease  of  the  nervous  system, 
the  localization  of  the  morbid  process  (nutritional), 
though  desirable,  is  much  less  important,  since  the  prog- 
nosis and  treatment  depend  on  other  indications.  It  is 
also  much  less  practicable,  and  is  at  best  uncertain,  since 
the  localization  depends  on  inferences  based  on  what  is 
known  of  the  effects  of  organic  lesions. 

It  is  inferred,  for  example,  that  certain  hysterical 
paralyses  depend  on  disease  (nutritional)  of  the  motor 
cortex,  because  it  is  known  that  organic  disease  of  the 
motor  cortex  gives  rise  to  symptoms  which  present  a 
close  resemblance  (segmental  distribution  of  palsy,  con- 
tractures, normal  electrical  reaction)  to  the  characters 
observed  in  functional  palsy.  The  following  review  of 
the  chief  manifestations  produced  by  disease  in  various 
parts  of  the  nervous  system  relates  exclusively  to  the 
effects  of  organic  processes.  The  chief  symptoms  of 
nervous  disease,  and  the  parts  concerned  in  their  produc- 
tion, have  already  been  considered,  and  it  is  necessary 
now  to  look  at  these  facts  from  another  point  of  view — 
to .  consider  the  symptoms  from  a  regional  standpoint. 
It  is  convenient  to  consider,  first,  the  chief  symptoms 
that  result  from  lesions  in  various  parts  of  the  brain  ; 
secondly,  the  symptoms  produced  by  disease  in  differ- 
This  relates  especially  to  operative  treatment. 


232         DISEASES   OF   THE   NERVOUS   SYSTEM. 

ent  regions  of  the  spinal  cord,  and  in  the  peripheral 
nerves. 

a.  Cortex  Cerebri. — i.  Destructive  disease  of  the 
Central  and  Motor  Area  of  the  brain  (anterior  and 
posterior  central  convolutions  and  paracentral  lobule, 
anterior  half  of  superior  parietal  lobule)  gives  rise  to 
hemiplegia  on  the  opposite  side  of  the  body. 

The  hemiplegia  is  usually  incomplete,  because  the 
lesion  more  often  involves  a  small  than  a  large  part  of 
the  central  area.  Partial  hemiplegia  (monoplegia)  occurs 
much  more  commonly  from  disease  of  the  cortex  than 
from  disease  more  deeply  seated  in  the  motor  path. 
Hence,  a  partial  paralysis,  if  due  to  brain  disease,  points 
to  the  existence  of  a  cortical  lesion. 

The  parts  that  suffer  from  the  palsy  vary  according  to 
the  position  of  the  lesion.  The  leg  suffers  alone  chiefly 
when  the  lesion  involves  the  paracentral  lobule,  or  the 
central  convolutions  close  to  the  longitudinal  fissure.  Il 
the  lesion  is  confined  to  that  part  of  the  leg  centre  which 
lies  in  the  upper  part  of  the  anterior  central  convolution, 
the  paralysis  probably  affects  mainly  the  foot.  If  the 
lesion  lies  between  the  longitudinal  fissure  and  the  junc- 
tion of  the  middle  with  the  lower  third  of  the  central 
convolutions,  there  is  paralysis  of  the  arm,  and  if  the 
lesion  involves  the  middle  third  only  of  these  convolu- 
tions, paralysis  of  the  arm  alone.  A  lesion  in  the  upper 
part  of  the  arm  centre  paralyzes  the  shoulder  more  than 
the  rest  of  the  arm.  A  lesion  in  the  very  lowest  part  of 
the  anterior  central  convolution  gives  rise  to  paralysis  of 
the  tongue  and  lips.  Any  slight  defect  in  articulation 
that  may  result  from  a  unilateral  lesion  in  this  situation 
is  transient,  being  soon  compensated  by  the  correspond- 
ing centre  in  the  opposite  hemisphere. 

In  cortical  disease  the  lesion  is  not  usually  confined  to 


DIAGNOSIS  OF  THE  POSITION  OF  THE  LESION.       233 

one  of  the  functional  areas  mentioned  (area  for  the  arm, 
or  leg,  or  face),  but  involves  adjacent  areas.  Hence  it  is 
that  paralysis  of  the  arm  and  leg,  or  of  the  face  and  arm, 
is  more  often  encountered  as  a  result  of  cortical  disease 
than  paralysis  of  one  of  these  parts  alone.  If  a  destruc- 
tive lesion  is  not  confined  strictly  to  the  cortex  (and  it 
usually  is  not),  it  may  involve  subjacent  white  tracts  from 
other  regions  of  the  cortex  which  are  not  the  seat  of  dis- 
ease, and  thus  give  rise  to  symptom.s  not  referable  to  the 
area  which  is  the  seat  of  the  cortical  lesion. 

In  addition  to  motor  paralysis,  lesions  of  the  cortex 
give  rise  very  often  to  convulsions.  This  is  the  case  with 
lesions  that  are  purely  irritative  in  character  and  with 
those  that  are  destructive  and  stationary  but  in  which 
the  destruction  is  partial  only.  The  convulsion  begins 
locally  in  the  leg,  arm,  or  face,  according  to  the  position 
of  the  disease  which  causes  it,  in  or  adjacent  to  the  area 
whose  destruction  gives  rise  to  motor  paralysis.  Such 
local  commencement  is  highly  suggestive  of  cortical  dis- 
ease. If  there  is  reason  to  regard  the  lesion  as  stationary — 
that  is,  no  longer  active  and  incapable  of  further  struc- 
tural recovery,  the  recurrence  of  local  convulsions  makes 
the  existence  of  cortical  disease  certain.  Their  recur- 
rence under  these  conditions,  however,  does  not  neces- 
sarily mean  that  the  region  of  the  cortex  corresponding 
to  the  locality  of  the  initial  spasm  is  the  part  most  dis- 
eased. A  lesion,  for  example,  situated  on  the  leg  centre 
may  give  rise  to  convulsions  beginning  in  the  face  or  arm 
centre,  because  the  disease  is  capable  of  starting  dis- 
charges from  adjoining  areas  which  are  less  diseased  but 
more  excitable. 

Localized  convulsion,  therefore,  is  to  be  regarded  as  a 
less  accurate  indication  of  the  exact  seat  of  the  lesion 
than  localized  motor  paralysis.     This  an  important  point. 


234         DISEASES   OF   THE   NERVOUS   SYSTEM. 

Disease  of  the  central  area  of  the  brain  very  often 
gives  rise  to  loss  of  sensation  in  the  extremity  of  the  part 
(or  parts)  paralyzed.  The  loss  of  sensibility  is  generally 
slight  in  degree.  It  involves  chiefly  tactile  sensibility, 
chiefly  marked  at  the  extremity  of  the  affected  limb, 
but  there  may  be  some  loss  of  pain  and  temperature 
sense.  Complete  hemiangesthesia  probably  never  results 
from  lesions  confined  to  the  motor  area.  The  sense  of 
posture  of  the  limbs  paralyzed  is  sometimes  impaired  in 
some  degree  by  lesions  of  the  motor  cortex  (especially 
its  posterior  part),  but  there  is  sometimes  a  similar  loss 
from  disease  of  the  motor  path  between  the  cortex  and 
the  lower  part  of  the  internal  capsule.  Lesions  of  the 
posterior  superior  parietal  lobule  also  cause  impairment 
of  the  sense  of  posture. 

2.  Lesions  of  the  Frontal  Lobe  of  the  brain,  anterior  to 
the  motor  area,  give  rise,  with  one  exception,  to  no  dis- 
tinctive focal  symptoms.  When  there  is  disease  of  the  pos- 
terior part  of  the  left  third  frontal  convolution  in  right- 
handed  persons  there  is  motor  aphasia.  A  lesion  in  the 
corresponding  position  in  the  right  frontal  lobe  produces 
the  same  effect  in  left-handed  persons.  Extensive  disease 
of  the  cortex  usually,  but  not  invariably,  causes  consid- 
erable mental  impairment,  as  shown  by  loss  of  memory 
and  attention,  and  sometimes  by  emotional  disturbance. 
Similar  mental  defect  may  result  from  extensive  cortical 
disease  in  other  parts  of  the  brain,  but  a  lesion  of  equal 
extent  probably  causes  less  impairment  than  is  produced 
by  disease  of  the  frontal  lobe.  Disease  in  the  posterior 
part  of  the  second  frontal  convolution  perhaps  gives  rise 
to  conjugate  deviation  of  the  eyes  and  head  (page  109). 
Disease  involving  the  frontal  lobes  in  such  a  way  as 
to  damage  the  olfactory  bulb  or  tract  causes  anosmia 
on  the  side  of  the  lesion. 

3.  The  precise  effects  of  lesions  of  the  Parietal  Lobe 


DIAGNOSIS  OF  THE  POSITION  OF  THE  LESION.       235 

posterior  to  the  motor  area  are  still  undetermined.  Le- 
sions of  the  posterior  portion  of  the  superior  parietal 
lobule  give  rise  to  loss  of  the  sense  of  posture  in  the  limbs 
of  the  opposite  side.  Disease  of  the  inferior  parietal 
lobule  probably  causes  ptosis  on  the  opposite  side,  but 
the  exact  area  on  which  this  depends  is  not  known.  It  is 
questionable  whether  lesions  of  the  angular  gyrus  which 
are  limited  to  the  cortex  are  competent  to  cause  crossed 
amblyopia,  but  it  is  probable  that  the  destruction  of  this 
region  on  the  left  side  causes  word-blindness  (p.  217). 
Destructive  disease  of  the  entire  parietal  lobe  generally 
impairs,  though  it  does  not  abolish,  sensibility  of  the  op- 
posite side  of  the  body  (trunk  and  limbs).  Lesions  in- 
volving both  the  parietal  lobe  and  the  motor  area  give 
rise  to  more  complete  hemianaesthesia  than  is  produced 
by  a  lesion  limited  to  either  region. 

4.  Lesions  of  the  cuneus  of  the  Occipital  Lobe  cause 
homonymous  hemianopsia.  Lesions  involving  the  upper 
and  lower  half  of  the  cuneus,  respectively,  are  probably 
capable  of  producing  partial  hemianopsia — that  is,  qua- 
drantic  homonymous  defects  (p.  165).  It  is  possible  that 
disease  just  anterior  to  the  half-vision  centre  (cuneus)  or 
in  its  anterior  part  may  give  rise  to  color  hemianopsia. 

Disease  of  the  external  surface  of  the  occipital  lobe 
seems  capable  of  causing  mind-blindness,  which  is  often 
associated  with  hemianopsia  from  involvement  of  the  sub- 
jacent visual  tract. 

5.  Lesions  involving  the  first  and  second  temporal 
convolutions  of  the  Temporo- Sphenoidal  Lobe  of  the  left 
side  give  rise  to  word-deafness.  Disease  of  the  posterior 
part  of  the  first  temporal  convolution  probably  gives 
rise  to  transient  deafness  in  the  opposite  ear,  and  an 
irritative  lesion  in  this  situation  may  give  rise  to  an 
auditory  aura. 


236        DISEASES   OF  THE   NERVOUS    SYSTEM. 

The  auditory  centre  in  man  cannot  at  present  be  very 
accurately  located. 

A  lesion  in  the  uncinate  convolution,  or  involving  the 
apex  of  the  temporo-sphenoidal  lobe  may  cause  marked 
disturbance  of  the  sense  of  smell.  Irritative  disease  in 
this  situation  may  determine  an  olfactory  aura. 

6.  Disease  of  the  Island  of  Reil  has  many  times  been 
associated  with  hemiplegia,  and  disease  extending  through 
the  insula  of  the  left  side  has  been  considered  effective  in 
producing  aphasia  by  interruption  of  the  path  between 
the  motor  and  auditory  speech  centres.  It  is  doubtful 
whether  hemiplegia  is  ever  the  effect  of  a  lesion  limited 
to  the  cortex  of  the  insula,  although  disease  of  the 
branches  of  the  middle  cerebral  artery,  as  they  pass  over 
the  insula,  may  undoubtedly  lead  to  lesions  elsewhere 
(motor  cortex  and  subjacent  white  substance)  that  pro- 
duce motor  paralysis.  It  also  remains  to  be  shown  that 
simple  interruption  of  the  path  beneath  the  insula,  above 
mentioned,  is  competent  by  itself  to  produce  amnesic 
aphasia. 

b.  White  Substance  and  Centrum  Ovale. — 
Disease  of  the  white  substance  of  the  hemisphere  and 
centrum  ovale  gives  rise  to  symptoms  referable,  on  the 
one  hand,  to  the  interruption  of  the  various  association 
tracts  which  connect  different  gyri  and  functional  areas 
of  the  cortex  with  one  another,  and,  on  the  other,  to  in- 
terruption of  tracts  which  have  a  peripheral  destination 
(projection  tracts).  Lesions  of  the  association  tracts,  if 
extensive,  probably  cause  mental  symptoms  chiefly,  loss 
of  memory  and  attention,  defective  will-control,  etc.  It 
is  doubtful  whether  any  lesions  of  this  kind  give  rise  to 
symptoms  that  possess  localizing  value.  Lesions  of  the 
tracts  which  connect  the  cortex  with  peripheral  nervous 
mechanisms  (retina,  motor  apparatus,  etc.)  produce  symp- 


DIAGNOSIS  OF  THE  POSITION  OF  THE  LESION.       237 

toms  which  resemble  those  that  result  from  disease  of  the 
region  of  the  cortex  with  which  the  particular  tracts  are 
connected.  Thus,  a  lesion  of  the  white  substance  of  the 
occipital  lobe,  involving  the  visual  path  to  the  cuneus, 
gives  rise  to  lateral  hemianopsia  ;  a  lesion  interrupting  the 
fibres  that  converge  from  the  central  area  of  the  cortex  to 
the  internal  capsule  gives  rise  to  hemiplegia.  The  various 
tracts  mentioned  all  converge  from  different  areas  of  the 
cortex,  widely  separated,  to  the  internal  capsule.  Hence, 
generally  speaking,  lesions  jus f  beneath  the  cortex  produce 
symptoms  like  those  dependent  on  disease  of  the  over- 
lying cortical  region,  while  those  that  approach  the  in- 
ternal capsule  produce  effects  like  those  of  capsular 
disease.  General  convulsions  are  not  common  in  disease 
of  the  white  substance  of  the  hemisphere,  even  when  such 
disease  is  irritative  in  character,  unless  it  be  placed  just 
beneath  the  cortex.  When  in  this  position  (particularly 
when  the  lesion  is  beneath  the  motor  cortex)  an  irritative 
lesion  (as  tumor)  often  gives  rise  to  the  local  spasm 
(Jacksonian  spasm)  which  is  so  characteristic  of  cortical 
disease.  The  motor  aphasia  which  follows  interruption 
of  the  path  from  the  motor  speech  region  (third  frontal 
gyrus)  to  the  internal  capsule  is  temporary,  except  when 
the  interruption  is  just  beneath  the  cortical  centre.  Con- 
jugate deviation  of  the  eyes  is  common  from  subcortical 
lesions. 

c.  Corpus  Callosum. — Lesions  are  so  rarely  limited 
to  the  corpus  callosum  that  the  diagnostic  indications  of 
its  damage  cannot  as  yet  be  formulated.  It  is  evident, 
however,  from  its  structure  that  it  associates  the  action 
of  the  two  hemispheres.  Bilateral  paresis  of  the  extremi- 
ties has  been  noted  in  many  cases  where  the  callosum 
was  damaged,  but  this  is  doubtless  referable  to  pressure 
upon  or  extension  into  the  motor  tract  in  the  cerebral 
hemispheres.      There    is    some    reason    to    believe    that 


238         DISEASES   OF  THE   NERVOUS   SYSTEM. 

destruction  of  the  anterior  extremity  of  the  callosum 
gives  rise  to  mental  diilness,  loss  of  memory,  and  other 
evidences  of  impaired  mental  power,  somewhat  similar 
to  that  noted  in  lesions  of  the  frontal  lobes. 

d.  Corpus  Striatum. — Disease  of  the  corpus  striatum 
(caudate  or  lenticular  nucleus)  causes  no  symptoms  that 
can  be  referred  to  damage  of  its  gray  substance.  Acute 
lesions  limited  to  either  nucleus  may  produce  transient 
hemiplegia,  but  this  symptom  is  doubtless  due  to  irritation 
of  the  adjacent  fibres  of  the  internal  capsule.  Chronic  dis- 
ease of  the  nuclei  produces  no  symptoms,  unless  the  motor 
or  sensory  fibres  of  the  internal  capsule  be  damaged  also. 

e.  Optic  Thalamus. — Most  of  the  symptoms  ob- 
served in  lesions  of  the  optic  thalamus  are  referable  to 
involvement  of  the  contiguous  internal  capsule  and  not  to 
the  direct  effect  of  the  thalamic  disease.  Thus,  the  hemi- 
plegia which  often  follows  disease  of  the  middle  third  of 
the  thalamus  is  due  to  implication,  often  slight,  of  the 
motor  fibres  of  the  capsule,  which  lie  just  external  to  this 
part  of  the  ganglion.  Similarly,  the  hemianaesthesia 
which  is  observed  to  accompany  disease  of  the  posterior 
extremity  of  the  thalamus  (pulvinar)  depends  not  on  the 
thalamic  lesion,  but  on  damage  to  the  sensory  part  of  the 
capsule.  Disease  of  the  middle  and  posterior  thirds  of 
the  thalamus  seems  to  be  directly  effective  in  producing 
inco-ordination  and  hemiathetosis  of  the  opposite  ex- 
tremities, but  it  cannot  be  denied  that  these  symptoms 
may  be  due,  at  least  in  part,  to  irritation  of  the  neighbor- 
ing motor  tract.  It  is  highly  probable  that  lateral  hemi- 
anopsia may  be  produced  by  a  destructive  lesion  limited 
to  the  pulvinar  of  the  thalamus,  and  that  the  symptom  is 
then  to  be  regarded  as  the  direct  result  of  this  destruction. 
The  association  of  hemianopsia  with  hemianaesthesia 
indicates  a  lesion  of  the  posterior  part  of  the  thalamus 
and  the  adjacent  sensory  fibres  of  the  internal  capsule. 


DIAGNOSIS  OF  THE  POSITION  OF  THE  LESION.      239 

The  so-called  basal  ganglia  probably  preside  over 
many  acts  which  are  commonly  performed  in  a  purely 
automatic  manner,  such  as  bodily  posture,  ordinary 
gait,  facial  expression,  and  probably  emotional  control. 
/.  Internal  Capsule. — Lesions  of  the  internal  cap- 
sule give  rise  to  symptoms  which  vary  much  according  to 
the  part  of  the  capsule  involved.  Disease  limited  to  the 
anterior  division  of  the  internal  capsule,  anterior  to  the 
knee  (between  the  caudate  and  lenticular  nuclei),  is  rare. 
and  does  not  give  rise  to  characteristic  symptoms.  Some- 
times mental  symptoms,  similar  to  those  referable  to  dis- 
ease of  the  frontal  lobe,  are  produced  by  disease  of  the 
anterior  part  of  the  capsule,  but  usually  it  seems  to  cause 
no  definite  effects.  Disease  involving  the  angle  (knee) 
and  the  anterior  two  thirds  of  the  posterior  division  of  the 
capsule  causes  hemiplegia  of  the  ordinary  variety — that  is, 
paralysis  of  the  opposite  leg,  arm,  and  face  (lower  part). 
If  the  lesion  is  on  the  left  side  there  is  frequently  motor 
aphasia,  but  this  is  always  transient.  If  the  lesion  be  of 
acute  onset  there  is  often  at  first  conjugate  deviation  of 
the  eyes,  to  the  hemiplegic  side  where  the  symptom  is  due 
to  irritation.  Sometimes  there  is  permanent  conjugate 
deviation.  This  is  usually  due  to  destruction,  and  the 
deviation  is  then  to  the  side  of  the  lesion  {^yide  p.  109). 
Convulsions  occasionally  attend  the  onset  of  hemiplegia 
from  disease  in  this  region.  They  seldom  recur  after  the 
onset.  Hemiathetosis  often  follows  incomplete  hemiplegia, 
but  it  is  not  certain  whether  the  symptom  is  referable  to  the 
capsular  disease  or  to  adjacent  disease  of  the  thalamus. 

The  hemiplegia  of  disease  of  the  internal  capsule  is 
usually  complete.  A  very  small  lesion,  limited  to  the 
angle  of  the  capsule,  may  give  rise  to  facial  paralysis 
only,  and,  similarly,  minute  lesions  in  the  anterior  and 
middle  thirds  respectively  of  the  posterior  division  of  the 
capsule,  may  produce  a  brachial  monoplegia  and  a  crural 


240        DISEASES   OF   THE   NERVOUS    SYSTEM. 

monoplegia.  It  is  exceedingly  rare,  however,  for  a  paraly- 
sis from  such  lesions  to  involve  exclusively  face,  arm,  or 
leg,  although  one  of  these  parts  may  be  chiefly  affected. 

Probably  three  fourths  of  all  cases  of  hemiplegia  result 
from  disease  of  the  internal  capsule  ;  hence,  in  the  ab- 
sence of  symptoms  pointing  to  another  locality  as  the  seat 
of  the  lesion,  there  is  always  a  strong  presumption  that  a 
hemiplegia  depends  on  damage  to  the  internal  capsule. 

Disease  of  the  posterior  third  of  the  posterior  division 
of  the  internal  capsule,  in  which  lies  the  sensory  tract, 
gives  rise  to  hemianaesthesia.  Taste,  hearing,  and  smell 
may  be  lost  on  the  anaesthetic  side,  as  the  paths  for  the 
special  senses  are  contiguous  to  the  path  for  common 
sensibility.  The  visual  path  is  also  involved  in  such  cases 
and  the  resulting  symptom  is  lateral  hemianopsia. 

g.  External  Capsule  and  Claustrum. — Lesions  of 
the  external  capsule  and  claustrum  do  not  give  rise  to 
distinctive  symptoms  and  cannot  therefore  be  localized. 

A.  Corpora  Quadrigemina. — Lesions  limited  to  the 
corpora  quadrigemina  are  of  exceedingly  rare  occurrence. 
Hence  there  is  still  considerable  doubt  as  to  the  precise 
effect  of  disease  in  this  situation.  Disease  of  the  ante- 
rior pair  has  been  thought  to  produce  blindness,  loss  of 
pupillary  reflex  and  nystagmus.  It  is  certain  that  there 
is  no  adequate  reason  to  suppose  that  blindness  is  ever 
directly  referable  to  disease  of  the  corpora  quadrigemina. 
Irritative  disease  (tumor)  of  the  quadrigeminal  region, 
like  such  disease  elsewhere,  may  give  rise  to  optic  neu- 
ritis and  secondary  optic  atrophy,  and  by  this  mechanism 
to  amblyopia,  but,  except  in  this  manner,  visual  acuity 
is  not  impaired.  There  has  been  no  impairment  of 
vision  even  in  cases  where  the  corpora  quadrigemina 
were  wholly  destroyed.  The  condition  of  the  pupillary 
reflexes  varies  so  much  in  different  cases  of  quadrigeminal 
disease  that  no  general  statement  can  be  made  regarding  it. 


DIAGNOSIS  OF  THE  POSITION    OF  THE  LESION.      24I 

It  is  probable  that  in  some  cases  of  such  disease  the 
reaction  to  light  is  lost.  Nystagmus  may  occur  from  irri- 
tative disease  of  the  quadrigeminal  region  as  from  irri- 
tative disease  in  other  regions.  It  probably  bears  no 
particular  relation  to  the  anterior  pair,  and,  as  elsewhere 
stated  (p.  129),  has  no  localizing  value.  Disease  of  the 
posterior  pair  has  many  times  been  associated  with  inco- 
ordination of  movement  (unsteadiness  in  walking  and 
standing,  reeling  or  staggering  gait),  and  is  probably,  in 
some  degree,  a  highly  constant  symptom  of  such  disease. 
It  must  be  owned  that  there  is  still  some  doubt  as  to 
whether  the  symptom  is  really  due  to  the  quadrigeminal 
disease  and  not  to  implication  of  the  middle  lobe  of 
the  cerebellum,  but  the  balance  of  evidence  is  much 
in  favor  of  the  former  view.  Paralysis  of  the  muscles 
supplied  by  the  oculomotorius  nerve  is  a  frequent  and 
important  symptom  of  disease  of  the  quadrigeminal 
region.  It  doubtless  depends  on  implication  of  the 
subjacent  nuclei  of  the  third  nerve  and  not  on  the 
quadrigeminal  disease  itself.  Usually  the  muscles  are 
neither  symmetrically  nor  equally  involved  in  the  paraly- 
sis, nor  are  they  all  implicated. 

While  it  is  impossible,  therefore,  to  localize  a  lesion  of 
one  or  other  pair  of  corpora  quadrigemina,  disease  of  the 
quadrigeminal  region  may  frequently  be  diagnosed  with 
accuracy.  The  symptoms  on  which  such  a  diagnosis  can 
be  made  are  the  coexistence  of  inco-ordination  of  move- 
ment (of  early  development  usually)  and  unsymmetrical 
and  incomplete  ophthalmoplegia  referable  to  the  oculo- 
motor nucleus. 

/.  Cms  Cerebri. — Lesions  of  the  crus  cerebri  (pes) 
frequently  cause  a  characteristic  combination  of  symp- 
toms— hemiplegia,  involving  the  lower  half  of  the  face 
and  the  limbs,  and  paralysis  of  the  third  nerve  on  the  side 

of  the  lesion — that  is  to  say,  on  the  side  opposite  the  hemi- 
16 


242         DISEASES   OF  THE   NERVOUS    SYSTEM. 

plegia  (crossed  or  "  alternate  "  hemiplegia).  Usually  the 
paralysis  of  the  third  nerve  is  complete  ;  occasionally  it 
is  partial.  It  is  important  to  bear  in  mind  that  if  the 
process  which  results  in  this  form  of  crossed  hemiplegia 
is  of  acute  onset,  the  lesion  cannot  be  referred  to  the  crus 
unless  both  hemiplegia  and  ocular  palsy  are  of  simul- 
taneous occurrence.  In  the  case  of  chronic  processes 
the  separate  development  of  the  two  symptoms  leaves  a 
doubt  as  to  whether  or  not  they  depend  on  the  same  lesion. 

Convulsions  are  rarely  observed  in  cases  of  disease 
of  the  crus.  Irritative  disease,  however,  may  give  rise 
to  rigidity.  If  the  lesion  involves  the  sensory  path  in  the 
tegmentum  of  the  crus,  anaesthesia  may  be  associated 
with  the  motor  paralysis.  Occasionally  (chiefly  in  irri- 
tative disease)  there  is  lateral  hemianopsia,  from  implica- 
tion of  the  contiguous  optic  tract.  Occasionally,  also, 
there  is  unilateral  inco-ordination. 

j.  Pons. — Lesions  of  the  pons  Varolii  generally  give 
rise  to  distinctive  symptoms.  Unilateral  disease  commonly 
involves  the  motor  path  to  one  side  of  the  body  and  cer- 
tain of  the  cranial  nerves  (fifth,  sixth,  or  seventh)  of  the 
other  side.  Several  different  varieties  of  crossed  hemi- 
plegia may  thus  arise  from  unilateral  pontine  disease, 
according  to  the  size  and  level  of  the  lesion.  Thus,  the 
limbs  may  be  paralyzed  on  one  side  and  the  face  on  the 
other — that  is,  on  the  side  of  the  lesion — by  a  lesion  which 
involves  the  facial  path  before  it  crosses  and  the  motor 
path  on  the  same  side.  In  this  case  the  entire  half  of  the 
face  is  paralyzed  and  the  muscles  give  the  R  D.  If  the 
lesion  is  near  the  median  line  and  near  the  middle  of  the 
pons,  it  may  be  so  placed  as  to  involve  the  facial  paths  of 
both  sides  with  the  motor  path  of  one  side.  Both  the 
sensory  and  motor  part  of  the  fifth  nerve,  or  either  alone, 
may  be  involved.  If  the  sensory  part  of  the  fifth  is  dam- 
aged by  an  irritative  lesion  there  is  severe  pain  on  one 


DIAGNOSIS  OF  THE  POSITION  OF  THE  LESION.       243 

side  of  the  face.  If  the  nucleus  of  the  sixth  nerve  of  one 
side  is  involved  in  a  destructive  lesion  there  is  conjugate 
deviation  of  both  eyes  to  the  side  opposite  to  the  lesion. 
This  implies  loss  of  function  of  the  internal  rectus  muscle 
which  habitually  acts  with  the  external  rectus  muscle 
(that  is,  the  internal  rectus  of  the  opposite  eye)  which  has 
been  paralyzed  by  destruction  of  the  nucleus  of  the  sixth 
nerve.  In  conjugate  movements  of  the  eyes  this  loss  of 
function  in  the  internal  rectus  exists,  although  for  other 
purposes  (convergence)  there  may  be  no  loss  of  power. 
Where  the  lesion  is  in  the  motor  path  of  the  pons  at 
the  level  at  which  the  sixth  nerve  traverses  the  pons  in 
passing  from  its  nucleus  to  the  surface,  the  nerve-trunk  is 
apt  to  be  involved.  Then  there  is  hemiplegia  with  paraly- 
sis of  the  external  rectus  on  the  side  of  the  lesion.  The 
associated  internal  rectus  of  the  other  eye  acts  normally, 
and  hence  there  is  no  conjugate  deviation  of  the  eyes. 

A  lesion  may  be  so  placed  in  the  motor  path  of  the 
pons  that  there  is  no  coincident  affection  of  any  of  the 
cranial  nerves.  In  such  cases  the  lesion  is  usually  above 
the  middle  of  the  pons — that  is,  in  a  part  of  the  pons  in 
which  the  upward  paths  from  the  nuclei  of  the  nerves  in 
question  have  already  crossed  to  the  opposite  side.  The 
resulting  hemiplegia  cannot  of  course  be  distinguished 
from  that  which  depends  on  capsular  disease. 

Bilateral  disease  of  the  pons  is  not  rare  and  may  give 
rise  to  a  variety  of  symptomatic  combinations.  A  lesion 
implicating  the  motor  path  of  both  sides  may  cause  com- 
plete paraplegia.  The  cranial  nerves  escape  or  are  bi- 
laterally involved  according  to  the  size  and  level  of  the 
lesion.  Bilateral  disease  of  acute  onset  usually  gives  rise 
to  apoplexy  and  often  to  rapid  death. 

Convulsions  are  uncommon  in  pontine  lesions  unless 
they  are  of  acute  onset.     Sometimes  the  convulsions  are 


244         DISEASES   OF   THE   NERVOUS   SYSTEM 

peculiar  in  distribution  ;  they  affect  chiefly  both  arms  or 
both  legs.  Irritative  processes  involving  both  pyramidal 
tracts  may  give  rise  to  rigidity  of  all  the  extremities. 
Tonic  spasm  is  very  often  met  with  in  partial  disease  of 
the  motor  path  within  the  pons,  and  may  correspond  in 
distribution  to  the  motor  paralysis.  Other  motor  symp- 
toms referable  to  irritation  (trismus  and  facial  spasm, 
choreic  movements)  are  rare. 

Lesions  involving  the  tegmental  region  of  the  pons, 
especially  the  formatio  reticularis  and  root  of  the  fifth 
nerve,  give  rise  to  loss  of  sensibility  in  the  limbs,  trunk, 
and  face.  A  unilateral  lesion  thus  placed  in  the  sensory 
path  in  the  upper  third  of  the  pons  may  cause  complete 
hemianaesthesia  on  the  side  opposite  the  lesion.  If  the 
lesion  is  below  the  upper  third  of  the  pons  and  damages 
the  sensory  path  from  the  face  and  limbs,  there  is 
"  crossed  "  anaesthesia — that  is,  anaesthesia  of  the  face  on 
the  side  of  the  lesion  and  of  the  limbs  on  the  opposite 
side  (see  page  145).  There  may  be  considerable  pain  in 
the  anaesthetic  side  of  the  face  in  these  cases.  Conjunc- 
tivitis sometimes  exists  on  the  side  of  the  lesion,  and 
there  may  be  unilateral  rhinitis.  These  symptoms  are 
apt  to  be  present  in  acute  processes  which  give  rise  to 
considerable  irritation.  Crossed  anaesthesia  is  sometimes 
associated  with  inco-ordination  of  one  or  both  lower  ex- 
tremities. Disease  involving  the  sensory  tract  of  both 
sides  gives  rise  to  bilateral  anaesthesia,  but  this  is  seldom 
complete. 

Unilateral  disease  limited  to  the  formatio  reticularis 
may  cause  only  anaesthesia  of  the  opposite  limbs  and 
trunk. 

Disease  of  the  posterior  part  of  the  pons  may  involve 
several  of  the  cranial  nerve  nuclei  and  give  rise  to  symp- 
toms referable  chiefly  to  their  implication.     A  combina- 


DIAGNOSIS  OF  THE  POSITION  OF  THE  LESION.       245 

tion  which  is  not  very  rare  is  paralysis  of  the  sixth  and 
seventh  without  the  auditory.  This  is  highly  character- 
istic of  pontine  disease.  Both  the  motor  and  sensory 
path  from  the  limbs  may  be  involved  by  a  large  unilateral 
pontine  lesion,  but  the  degree  and  extent  of  the  anaesthesia 
and  motor  palsy  are  seldom  proportioned.  This  depends 
on  the  fact  that  the  two  paths  are  separated  from  one 
another  by  the  considerable  interval  occupied  by  the  deep 
transverse  fibres  of  the  pons  (see  Fig.  4). 

Acute  irritating  processes  (especially  hemorrhage)* 
particularly  in  the  upper  part  of  the  pons,  often  cause 
contraction  of  the  pupils  by  their  indirect  effect  on  the 
oculomotorius  nuclei.  Disturbance  of  respiration,  tem- 
porary but  often  grave,  may  result  from  acute  lesions  of 
the  pons  in  almost  any  situation.  Cardiac  disturbance  is 
less  frequent.  Deafness  is  uncommon  in  pontine  lesions, 
and  taste  is  not  often  affected.  Sight  may  be  impaired  as 
a  result  of  optic  neuritis,  never  as  a  direct  consequence 
of  pontine  disease.  If  the  lesion  encroaches  on  the  mid- 
dle peduncle  of  the  cerebellum  there  may  be  a  tendency 
to  rotation  to  the  side  of  the  lesion  in  walking  and  severe 
giddiness  at  the  onset  of  an  acute  process.  Hyperpyrexia 
not  infrequently  follows  acute  lesions  of  the  pons,  and  in 
itself  suggests  pontine  or  medullary  disease.  Lesions  of 
considerable  size  in  the  pons  sometimes  cause  much 
psychical  disturbance. 

The  most  frequent  characteristic  symptoms  of  pontine 
disease  are  the  crossed  motor  paralyses  already  described. 
When  such  a  paralysis  occurs  suddenly  it  is  practically 
pathognomonic  of  a  lesion  of  the  pons.  Crossed  anaesthesia 
is  much  less  frequent  than  the  crossed  motor  palsies,  and 
may  result  from  disease  of  the  upper  part  of  the  medulla, 
but  its  occurrence  makes  a  pontine  lesion  practically  cer- 
tain.      In    the   absence    of   any    of   these    characteristic 


•"fftm^ 


'Hftitft 


DIAGNOSIS  OF  THE  POSITION  OF  THE  LESION.       247 

be  either  bilateral  or  unilateral.  When  bilateral,  either 
the  upper  or  lower  extremities  may  be  chiefly  involved  in 
the  paralysis  and  spasm.  A  small  chronic  lesion  (tumor) 
may  damage  the  pyramidal  tract  above  the  decussation 
and  the  hypoglossal  nerve  of  the  same  side.  The  result- 
ing variety  of  crossed  hemiplegia  (paralysis  of  the  tongue 
and  limbs  on  opposite  sides)  is  distinctive  of  disease  of 
the  medulla.  The  tongue  in  such  a  case  deviates  to  the 
side  opposite  the  limbs  palsied.  This  form  of  crossed 
paralysis  is  much  less  frequent  than  the  crossed  seventh 
and  limb  palsy  that  occurs  from  pontine  disease.  The 
face  is  never  implicated  in  a  lesion  of  the  medulla,  but 
the  orbicularis  oris  may  be  involved,  since  it  is  innervated, 
not  by  the  seventh  nerve,  but  by  the  hypoglossal  nucleus 
or  cells  connected  with  it. 

Lesions  of  the  medulla  in  some  cases  cause  paralysis  of 
motion,  or  paralysis  of  sensation,  or  both,  according  to 
the  situation  of  the  lesion  in  the  motor  or  sensory  tract, 
without  giving  rise  to  symptoms  that  are  characteristic  of 
or  even  suggest  medullary  disease.  Glycosuria  and  poly- 
uria are  occasionally  observed  in  the  course  of  chronic 
lesions  (tumor)  involving  the  floor  of  the  fourth  ventricle, 
but  the  causation  of  these  symptoms  is  too  obscure  and 
their  occurrence  too  inconstant  to  make  them  of  diag- 
nostic value. 

/.  Cerebellum. — A  destructive  lesion  of  consider- 
able size  involving  the  Middle  Lobe  of  the  cerebellum  gives 
rise  to  unsteadiness  in  standing  and  walking.  In  walking 
the  patient  may  grope  about  with  the  feet  widely  sepa- 
rated, the  hands  extended,  and  the  body  inclined  forward. 
The  tendency  to  oscillation  may  make  progress  so  irregu- 
lar that  the  gait  resembles  that  of  a  drunken  man.  This 
titubation  is  sufficiently  characteristic  and  frequent  to 
make  it  suggestive  of  cerebellar  disease.     Occasionally 


248        DISEASES   OF  THE   NERVOUS   SYSTEM. 

the  gait  of  tabes  resembles  cerebellar  titubation,  but  in 
disease  of  the  middle  lobe  there  is  not  the  ataxia  that 
characterizes  locomotor  ataxia.  There  is  also  usually 
no  inco-ordination  in  the  upper  extremities,  closure  of  the 
eyes  may  not  increase  the  unsteadiness,  and  there  may 
be  no  ataxia  whatever  in  the  upper  or  lower  extremities 
when  the  patient  lies  supine.  Occasionally  disease  of  the 
middle  lobe  causes  a  tendency  to  fall  backwards  when 
the  patient  attempts  to  stand. 

In  irritative  disease  of  the  middle  lobe  of  the  cerebel- 
lum (tumor,  hemorrhage,  softening),  giddiness  and  vertigo 
are  of  frequent  occurrence.  The  giddiness  may  or  may 
not  be  associated  with  titubation  or  staggering.  Vomit- 
ing is  also  a  frequent  symptom  of  active  cerebellar  dis- 
ease, but  both  vomiting  and  giddinesss  are  often  caused 
by  disease  in  other  parts  of  the  brain.  Hence,  although 
these  symptoms  are  distinctly  more  constant  in  cerebellar 
disease  than  in  disease  elsewhere,  they  possess  only  a 
slight  degree  of  localizing  value.  Optic  neuritis  is  per- 
haps somewhat  more  constant  in  cerebellar  disease  than 
in  similar  disease  elsewhere,  and  is  often  an  early  symptom. 

Disease  of  the  lateral  lobes  or  hemispheres  of  the  cere- 
bellum probably  gives  rise  to  no  symptoms  of  localizing 
significance,  unless  it  involves  the  middle  peduncles  or 
exerts  pressure  on  the  middle  lobe  of  the  cerebellum. 
In  the  latter  case  the  symptoms  are  those  referable  to 
disease  of  the  middle  lobe. 

Irritative  lesions  of  the  cerebellum  ( especially  tumor  ) 
sometimes  inhibit  temporarily  the  spinal  reflex  centres  on 
which  the  knee-jerk  depends,  so  that  the  knee-jerk  may 
be  lost  or  very  much  diminished.  In  some  instances  the 
knee-jerk  is  lost  for  days  or  weeks  and  then  reappears,  to 
be  lost  again  after  a  variable  period  of  time.  The  knee- 
jerks   may   be    unequal     in    activity     on    the  two  sides. 


DIAGNOSIS  OF  THE  POSITION  OF  THE  LESION.      249 

Sometimes  the  knee-jerks  are  diminished  for  a  long  period 
of  time.  It  is  not  known  whether  this  unique  symptom 
is  related  to  disease  of  any  particular  region  of  the  cere- 
bellum. In  cases  of  chronic  organic  intracranial  disease, 
in  which  indications  of  the  position  of  the  lesion  are 
absent,  the  occurrence  of  this  symptom  suggests  a  cer- 
ebellar process. 

Disease  ( tumor )  of  the  middle  or  lateral  lobes  of  the 
cerebellum  may  exert  pressure  on  surrounding  parts, 
particularly  on  the  pons.  The  symptoms  referable  to 
such  pressure  are  mainly  the  symptoms  of  pressure  on 
one  or  both  pyramidal  tracts — slight  or  considerable 
weakness  of  the  extremities,  increased  knee-jerk,  etc. 
Usually  the  symptoms  are  most  marked  on  the  side 
opposite  the  cerebellar  lesion  ;  sometimes  they  are  con- 
fined to  the  same  side.  Sometimes  there  is  also  evidence 
of  implication  in  the  sensory  -paths  in  the  pons,  slight 
anaesthesia,  paraesthesia,  etc.  There  is  seldom  sufficient 
pressure  to  cause  more  than  slight  and  transient  sensory 
disturbance.  Sometimes  the  cranial  nerves  arising  from 
the  pons  suffer  from  the  pressure.  The  sixth  nerve  is 
particularly  apt,  on  account  of  its  passage  under  the 
prominence  of  the  pons,  to  be  involved.  Convulsion  is 
of  rare  occurrence  in  cerebellar  disease.  Rigidity  of  the 
limbs  and  muscles  of  the  back  of  the  neck  may  occur, 
as  a  temporary  or  as  a  constant  phenomenon.  It  is  prob- 
ably dependent  on  pressure  exerted  upon  the  pons. 

It  is  important  to  remember  that  even  extensive  lesions 
of  the  cerebellar  hemisphere  may  produce  no  symptoms 
that  suggest  intracranial  disease,  but  this  is  probably  the 
case  only  in  very  chronic  processes  which  cause  little  irri- 
tation (for  example,  osteoma  and  some  cases  of  massive 
tubercle). 

Active  disease  of  the  Middle  Peduncle  of  the  Cerebellum 


250        DISEASES   OF  THE  NERVOUS   SYSTEM. 

(processus  ad  pontem)  almost  invariably  gives  rise  to 
distinctive  symptoms.  The  most  important  of  these  is 
vertigo,  which  is  often  intense,  and  a  tendency  to  rotation 
of  the  body  on  its  long  axis  (forced  or  compulsory  move- 
ments), to  or  from  the  sides  of  the  lesion,  or  simply  a 
tendency  to  lie  on  one  side,  or  rotate  to  one  side  in 
walking. 

A  lesion  seldom  involves  exclusively  the  middle  cere- 
bellar peduncle  ;  it  usually  encroaches  on  the  side  of  the 
pons  or  on  the  corresponding  hemisphere  of  the  cerebel- 
lum. In  the  former  case  there  may  be  paralysis  of  the 
fifth  nerve,  and,  if  the  motor  tract  is  compressed,  uni- 
lateral weakness  of  the  limbs.  Stationary  disease  of  the 
middle  peduncle,  and  lesions  which  simply  exert  pressure 
on  it,  may  cause  no  characteristic  symptoms. 

Disease  at  the  Base  of  the  Brain  (tumor,  meningitis) 
often  produces  symptoms  which  are  highly  characteristic. 
This  depends  chiefly  on  the  circumstance  that  in  most 
instances  basal  disease  damages  two  or  more  of  the 
cranial  nerves  between  their  superficial  origin  from  the 
brain  and  their  exit  from  the  skull,  thus  giving  rise  to 
symptom-groups  which  possess  localizing  value.  It  is 
convenient  to  consider  separately  the  symptoms  of  basal 
disease  in  the  anterior,  middle,  and  posterior  fossae  of  the 
skull. 

Disease  may  be  limited  to  the  Anterior  Fossa  of  the 
skull,  in  which  case  it  may  produce  symptoms  referable 
to  damage  of  the  olfactory  nerves,  or,  if  the  process 
compresses  or  invades  the  frontal  lobes,  there  may  be 
mental  symptoms.  Frequently  morbid  processes  origi- 
nating in  the  anterior  fossa  extend  backwards  and  involve 
the  optic  nerve  or  chiasm.  Implication  of  the  optic 
nerve  is  usually  unilateral,  and  causes  unilateral  ambly- 
opia or  amaurosis.     Damage  to  the  chiasma  may  affect 


DIAGNOSIS  OF  THE  POSITION  OF  THE  LESION.       25  I 

chiefly  the  decussating  fibres,  with  resulting  temporal 
hemianopsia. 

Disease  in  the  Middle  Fossa  causes  symptoms  referable 
chiefly  to  the  fifth  nerve.  The  Gasserian  ganglion  is 
usually  involved,  and  all  three  divisions  of  the  nerve  are 
apt  to  be  damaged,  though  they  may  suffer  singly  or 
unequally.  The  symptoms  may  be  those  of  irritation  or 
of  paralysis  (pain  or  anaesthesia)  of  the  nerve.  When 
the  Gasserian  ganglion  is  damaged  there  is  neuro- 
paralytic ophthalmia,  and  the  association  of  this  symptom 
with  symptoms  of  irritation  and  paralysis  of  the  fifth  is 
highly  distinctive  of  disease  of  the  middle  fossa.  The 
symptoms  are,  of  course,  unilateral.  Sometimes  the  crus 
is  involved  by  extension  ;  there  may  then  be  hemiplegic 
weakness.  Occasionally  the  third,  fourth,  and  sixth 
nerves  of  one  side  suffer  damage  from  disease  near  the 
sphenoidal  fissure. 

Disease  in  the  Posterior  Fossa  of  the  skull  causes'  com-, 
binations  of  symptoms  that  resemble  those  produced  by 
disease  within  the  pons  and  medulla,  with  similar  varia- 
tions according  to  the  position  at  which  the  process  is 
effective.  There  are  two  facts,  however,  which  generally 
serve  to  distinguish  disease  originating  in  the  posterior 
fossa  from  that  which  involves  the  pons  and  medulla 
primarily.  First,  the  combinations  of  the  cranial  nerves 
that  can  be  damaged  by  disease  are  different  in  the  two 
cases;  and  secondly,  when  there  is  disease  in  the  fossa 
the  cranial  nerves  are  prone  to  suffer  before  there  is 
evidence  of  damage  to  the  motor  path  in  the  pons  and 
medulla. 

In  basal  disease  the  fifth  and  sixth  nerves  readily  suf- 
fer together,  since  the  sixth  in  its  course  passes  close  to 
the  former.  This  combination  is  exceedingly  rare  in 
pontine  disease.     The  seventh  and  eighth  readily  become 


252         DISEASES   OF   THE   NERVOUS   SYSTEM. 

involved  together  in  disease  at  the  base,  while  the  same 
combination  is  possible  only  in  very  extensive  disease  of 
the  pons.  Similarly,  but  more  rarely,  the  sixth,  seventh 
and  eighth  are  damaged  together.  The  eleventh  and 
twelfth  or  the  ninth,  eleventh,  and  twelfth  may  be  injured 
together.  In  the  latter  case  there  is  unilateral  paralysis 
of  the  tongue,  palate,  and  vocal  cord — a  combination, dis- 
tinctive of  disease  at  the  side  of  the  medulla.  Disease 
of  the  same  parts  from  a  central  lesion  is  generally  bi- 
lateral, and  is  associated  with  palsy  of  the  lips.  Occa- 
sionally, many  cranial  nerves  are  damaged  by  a  process 
(chronic  meningitis)  in  the  posterior  fossa.  Thus,  the 
fifth,  sixth,  seventh,  eighth,  ninth,  tenth,  eleventh,  and 
twelfth  have  been  known  to  be  involved  on  one  side. 
The  number  of  nerves  involved  in  a  basal  lesion,  and  the 
order  and  degree  of  their  implication,  are  subject  to  great 
variations.  The  cranial  nerve  paralyses  from  disease  of 
the  posterior  fossa  are  rarely  strictly  unilateral  through- 
out the  disease.  When  the  fifth  is  involved  there  may 
be  ophthalmitis,  but  this  is  less  frequent  than  in  disease 
of  the  middle  fossa.  The  motor  path  is  often  involved 
unilaterally,  with  the  usual  results.  Occasionally  the 
middle  cerebellar  peduncle  suffers  from  pressure.  Con- 
vulsions may  result  from  pressure  on  the  pons,  but  these 
possess  no  distinctive  character  from  those  which  result 
from  disease  in  its  substance. 

Having  passed  in  review  the  chief  symptoms  of  brain 
disease  in  their  relation  to  the  position  of  the  lesion,  it 
becomes  necessary  to  mention  certain  general  facts  of 
diagnosis  which  are  of  importance  in  forming  correct 
conclusions  in  localization.  In  any  case  of  brain  disease 
in  which  the  symptoms  are  of  acute  onset  it  is  necessary 
to  distinguish  the  indirect  from  the  direct  effects  of  the 
lesion.     This  can  be  done  surely  only  by  waiting  until 


DIAGNOSIS  OF  THE  POSITION  OF  THE  LESION.       253 

the  indirect  symptoms  have  disappeared  or  diminished 
greatly,  and  this  usually  occurs  in  the  course  of  ten 
days  or  two  weeks.  In  this  way  the  symptoms  that  de- 
pend on  actual  destruction  of  tissue  may  be  certainly 
distinguished  from  those  that  result  from  irritation,  and 
the  distinction  is  important,  not  only  for  accurate  local- 
ization, but  for  prognosis.  Of  course,  a  prediction  can 
be  made  soon  after  the  development  of  the  symptoms,  as 
to- which  symptoms  are  direct,  but  at  best  the  truth  can 
only  be  approximated.  In  the  case  of  chronic  lesions 
(tumor)  which  both  irritate  and  destroy,  the  distinction 
is  often  difficult  and  may  make  a  nice  localization  im- 
possible. A  second  point  of  importance  relates  to  the 
order  of  appearance  of  the  different  symptoms.  It  is  es- 
pecially desirable  to  note  this  in  the  case  of  acute  lesions, 
since  only  such  symptoms  as  make  their  appearance  together 
are  to  be  referred  to  the  same  focus  of  disease.  When  all 
the  symptoms  are  of  gradual  onset  it  may  be  difficult  to 
determine  whether  they  are  to  be  referred  to  the  same  or 
to  different  lesions.  Multiple  lesions  of  the  brain  are 
usually  difficult  to  localize  accurately,  since  they  are  apt 
to  produce  combinations  of  symptoms  that  are  of  doubt- 
ful significance.  If,  however,  there  are  two  lesions  in  op- 
posite halves  of  the  brain,  it  is  frequently  an  easy  matter 
to  localize  them,  especially  if  they  are  not  simultaneous  in 
their  development.  In  any  case  it  is  exceedingly  import- 
ant to  determine  accurately  the  mode  (whether  sudden 
or  gradual)  and  order  of  development  of  the  symptoms, 
before  formulating  a  conclusion  as  to  the  locality  of  the 
lesion. 

Spinal  Cord. — The  localization  of  lesions  of  the 
spinal  cord  is  in  many  respects  less  difficult  than  the 
localization  of  lesions  of  the  brain.  This  depends  chiefly 
on  the  fact  that  even  a  small  focus  of  disease  in  the  sub- 


254         DISEASES   OF   THE   NERVOUS   SYSTEM. 

Stance  of  the  cord  almost  invariably  interrupts  structures 
that  have  important  motor  or  sensory  functions,  the  dis- 
turbance of  which  indicates  approximately  or  accurately 
the  position  of  the  morbid  process. 

Most  diseases  of  the  spinal  cord  involve  a  part  only  of 
its  substance.  Some  lesions  damage  a  considerable  cxt 
tent  of  certain  structures,  white  or  gray,  without  invading 
adjacent  structures.  The  term  "  system-diseases  "  has 
been  applied  to  such  lesions.  Other  lesions  are  of  small 
vertical  extent,  and  may  be  confined  to  particular  struc- 
tures, as  the  ganglion-cells  of  the  anterior  horns  or  the 
pyramidal  tracts,  or  may  damage  all  the  structures  of  the 
cord  at  a  particular  level.  Lesions  which  are  limited 
both  in  vertical  and  horizontal  extent  are  called  ''focal  " 
lesions.  The  problem  of  localization  includes  the  deter- 
mination of  both  the  vertical  and  horizontal  extent  of  the 
lesion.  The  indications  of  the  horizontal  extent  of  the 
lesion  depend  on  the  fact  that  different  areas  of  the 
white  and  gray  substance  at  the  same  level  have  widely 
different  functions. 

I.  Lesions  involving  the  Gray  Substance  of  the  spinal 
cord  produce  different  symptoms  according  as  the  morbid 
process  involves  (<2)  the  anterior  horns,  {]?)  the  posterior 
horns,  or  (r)  both  anterior  and  posterior  horns. 

Disease  of  the  Anterior  Horns  ^nq^  rise  to  three  distinct 
results.  There  is,  first,  motor  paralysis.  This  depends 
on  the  fact  that  destruction  of  the  ganglion-cells  of  the 
anterior  horns  constitutes  an  interruption  of  the  motor 
path  from  the  cerebral  cortex  to  the  muscles.  \w  addition 
to  motor  paralysis  there  is  degenerative  atrophy  of  the 
paralyzed  muscles  with  R  D.  The  combination  of  par- 
alysis with  degenerative  atrophy  always  localizes  the 
lesion  to  some  part  of  the  lower  segment  of  the  motor 
path.     The   third  result  of  disease  of  the  anterior  horn 


DIAGNOSIS  OF  THE  POSITION  OF  THE  LESION.       255 

is  loss  or  impairment  of  reflexes  in  which  the  muscles 
paralyzed  are  concerned.  The  clinical  type  of  paralysis 
resulting  from  disease  of  the  anterior  horns  may  be 
termed  atrophic  spinal  paralysis. 

The  distribution  of  these  symptoms  depends  on  the 
level  of  the  spinal  cord  at  which  the  ganglion-cells  are 
involved,  and  on  the  extent  of  the  damage  in  a  vertical 
direction.  The  special  symptoms  of  anterior  cornual 
disease  at  various  levels  will  be  considered  later. 

If  the  lesion  of  the  anterior  horn  is  of  acute  onset  (for 
example,  poliomyelitis)  the  loss  of  voluntary  power  is 
also  of  rapid  development.  Degenerative  atrophy  fol- 
lows, and  the  atrophy  and  altered  electrical  reactions 
become  apparent  in  the  course  of  one  or  two  weeks. 
When  the  lesion  is  of  gradual  development  (progressive 
muscular  atrophy)  the  paralysis  and  atrophy  develop 
[  pari  passu. 

Disease  limited  strictly  to  the  anterior  horn  does  not 
give  rise  to  sensory  symptoms,  and  the  absence  of  such 
symptoms  seems  to  distinguish  disease  of  the  anterior 
horns  from  disease  of  other  parts  of  the  lower  segment  of 
the  motor  path.  Paralysis,  wasting,  and  loss  of  reflex 
action  are  symptoms  common  to  disease  i)i  any  part  of  the 
lower  segmeiit  of  the  motor  path,  but  disease  of  the  periph- 
eral part  of  the  path  is  usually  (not  always)  associated 
with  sensory  symptoms — numbness,  tingling,  anaesthesia, 
etc. — because  the  motor  fibres  are  mixed  with  sensory 
fibres,  and  the  former  seldom  suffer  alone. 

When  an  acute  lesion  of  the  anterior  horns  is  accom- 
panied with  sensory  symptoms,  these  are  due  to  damage, 
often  slight,  to  adjacent  sensory  structures.  At  the 
onset  of  an  acute  lesion  of  the  anterior  comua  spasm 
may  be  a  prominent  symptom. 

Disease  limited  to  the  structures  of  the  Posterior  Horn 


256        DISEASES   OF   THE   NERVOUS   SYSTEM. 

is  exceedingly  rare,  and  there  is  some  uncertainty  as  to  the 
exact  character  of  the  symptoms  that  result  from  such  dis- 
ease. Irritative  disease  probably  gives  rise  to  pain,  and 
perhaps  to  hyperalgesia,  in  a  corresponding  skin  area. 
Destructive  disease  probably  causes  loss  of  certain  forms 
of  sensibility,  especially  the  sensibility  to  pain  and  tem- 
perature. It  is  very  doubtful  whether  tactile  sensibility 
or  the  muscular  sense  are  ever  disturbed. 

Chronic  lesions  (chiefly  gliomatous  infiltration  and 
cavity  formation)  involving  both  Anterior  and  Posterior 
horns  of  gray  matter  are  occasionally  observed.  They 
are  characterized  by  the  development  of  muscular  atro- 
phy with  R  D,  gradual  loss  of  voluntary  power,  and  dis- 
turbances of  sensibility,  not  for  touch,  but  for  pain 
and  temperature.  Since  these  sensory  disturbances  are 
not  obtrusive  they  may  be  overlooked  unless  they  are 
especially  sought  for,  and  the  symptoms  (atrophy  and 
wasting,  etc.)  may  be  referred  to  the  anterior  horns 
(progressive  muscular  atrophy).  The  chief  condition 
that  gives  rise  to  this  characteristic  combination  of 
motor  and  sensory  symptoms  mentioned  is  syringomyelia 

(p.  488). 

2.  White  Matter. — Disease  of  the  Anterior  and  Lateral 
White  Columns  of  the  cord  gives  rise  to  a  characteristic 
group  of  symptoms.  There  is,  first,  loss  of  voluntary 
power  below  the  level  of  the  lesion.  This  loss  of  power 
is  not  associated  with  degenerative  atrophy  of  the  mus- 
cles. Secondly,  there  is  excessive  action  of  the  spinal 
centres  (ganglion-cells  of  anterior  gray  cornua)  below 
the  lesion.  This  is  manifested  by  the  presence  of  two 
symptoms,  (^)  excessive  reflex  action,  shown  especially 
by  increase  in  the  knee-jerk,  Babinski's  sign,  and 
often  by  the  presence  of  an  ankle  clonus,  and  {h)  spasm 
or  rigidity  of  the  muscles  below  the  seat  of  the  disease. 


DIAGNOSIS  OF  THE  POSITION  OF  THE  LESION.       257 

The  former  symptom  may  be  present  without  the  latter 
where  the  excess  is  not  great,  but  in  many  cases  both 
expressions  of  the  overaction  of  the  spinal  centres  are 
present.  The  clinical  type  of  paralysis  that  results  from 
disease  of  the  lateral  columns  is  called  spastic  spinal 
paralysis.  When  only  the  anterior  and  lateral  columns 
are  involved  in  disease  there  is,  as  stated  above,  no  de- 
generative atrophy.  If,  however,  the  ganglion-cells  of 
the  anterior  horns  suffer  also,  as  they  may,  degenerative 
atrophy  occurs  in  the  muscles  connected  with  them,  and 
with  this  there  is  diminution  or  loss  of  reflex  action, 
notwithstanding  the  fact  that  reflex  action  may  previously 
have  befen  increased. 

The  symptoms  described  as  evidence  of  disease  of  the 
anterior  and  lateral  columns  depend  on  the  involvement 
of  the  pyramidal  tracts.  We  cannot  yet  say  precisely 
what  symptoms  are  produced  by  lesions  involving  the 
other  important  conducting  tracts  of  these  columns, 
(direct  cerebellar  tract,  antero-lateral  tract). 

It  is  evident  from  what  has  gone  before  that  two  dis- 
tinct clinical  types  of  paralysis  (atrophic  spinal  paralysis, 
spastic  spinal  paralysis)  may  result  from  spinal-cord 
lesions,  according  as  the  morbid  process  involves  the 
anterior  horns  or  the  pyramidal  tracts  of  the  anterior  and 
lateral  columns.  The  clinical  features  of  these  forms, 
which  are  sometimes  blended,  are  elsewhere  enumerated 
(see  Chap.  V.). 

Disease  confined  to  the  Postero- External  Column  of  the 
posterior  column  of  the  cord  gives  rise  to  distinctive  symp- 
toms. These  are  (i)  inco-ordination  in  the  extremities 
below  the  level  of  the  lesion  ;  (2)  loss  of  tactile  sensibility, 
varying  in  distribution  (usually  chiefly  in  the  legs)  accord- 
ing to  the  vertical  extent  and  position  of  the  lesion  ;  and 
(3)  diminution  or  loss  of  reflex  action  (loss  of  knee-jerk 

if   the  lesion  is  in  the  lumbar  cord).     These  symptoms 
17 


258         DISEASES   OF   THE   NERVOUS   SYSTEM. 

depend  on  the  fact  that  the  postero-external  columns  con- 
tain many  of  the  fibres  of  the  posterior  nerve-roots  which 
are  necessarily  interrupted  by  a  morbid  process  in  the 
former  situation.  The  posterior  nerve-roots  are  often 
diseased  by  degenerative  processes  that  involve  the 
postero-external  columns,  and  give  rise  to  similar  and 
sometimes  identical  symptoms — with  the  exception  that 
pain  is  often  a  prominent  feature  in  nerve-root  disease 
(the  path  for  painful  stimuli  being  contained  in  these 
roots),  while  it  is  open  to  question  whether  disease  limited 
to  the  postero-external  columns  causes  pain. 

Disease  limited  to  the  Poster o-Internal  Columns  of  the 
cord  (columns  of  Goll)  is  exceedingly  rare,  but  disease 
of  these  columns  secondary  to  disease  (usually  degenera- 
tive) of  the  postero-external  columns  is  not  of  infrequent 
occurrence.  There  is  little  clinico-pathological  evidence 
to  show  what  symptoms  result  from  disease  in  this  posi- 
tion, but  it  is  on  the  whole  probable  that  it  gives  rise  to 
disturbance  of  co-ordination  or  of  equilibrium.  Ordi- 
narily any  disturbance  of  this  nature  must  be  masked  by 
the  inco-ordination  that  results  from  the  disease  of  the 
postero-external  columns,  to  which  lesions  of  the  posterior 
median  columns  are  secondary. 

A  Unilateral  Lesio7i  of  the  spinal  cord  gives  rise  to  a 
highly  characteristic  group  of  symptoms.  First,  there  is 
motor  paralysis  on  the  side  of  the  lesion  and  below  its 
level.  This  depends  on  the  interruption  of  the  fibres  of 
the  pyramidal  tracts.  Often  there  is  slight  weakness  on 
the  opposite  side,  usually  of  the  leg.  Secondly,  there  is 
loss  of  sensibility  on  the  side  opposite  the  lesion.  The  loss 
of  sensibility  does  not  extend  quite  as  high  as  the  level  of 
the  lesion.  This  is  because  the  sensory  path  does  not 
decussate  immediately  at  the  level  of  the  entrance  of  the 
sensory  nerves,  but  a  short  distance  above  this.     There  is 


DIAGNOSIS  OF  THE  POSITION  OF  THE  LESION.       259 


MOTOR 
TRACT 


(^■N  E.  RA  l_ 


SENS.TRAtT 
TRACT 


tflusci.e  $£NS£: 


sewSoRY 


,M0TOR. 


FIG.    71. 

Diagram  showing  the  arrangement  of  the  sensory  and  m  tor  tracts  in  the 
cord  and  medulla  and  the  effects  of  a  unilateral  lesion.  R,  R,  R,  nerve-roots. 
The  sensory  paths  are  represented  in  red,  the  motor  paths  in  black.  It  is  tc 
be  noted  that  the  tracts  conveying  general  sensibility  cross  to  the  opposite  side 
of  the  cord  soon  after  entering  it,  while  the  tracts  conveying  muscular  sensi- 
bility cross  in  the  niedulla  just  above  the  motor  decussation.  The  nerve-roots 
are  to  be  considered  in  the  dorsal  cord,  the  cervical  cord  being  left  out.  A 
unilateral  lesion  in  the  dorsal  region  of  the  cord  would  produce  the  following 
effects  .  Paralysis  of  motion  on  the  same  side  (leg),  loss  of  muscular  sense  in 
the  same  side  in  the  parts  below,  loss  of  sensation  on  the  opposite  side  (leg) 
below  the  lesion. 


26o         DISEASES   OF   THE   NERVOUS   SYSTEM. 

one  exception  to  the  rule  that  sensation  is  affected  on  the 
side  opposite  a  unilateral  lesion  of  the  cord.  This  relates 
to  one-sided  lesions  of  the  lumbar  enlargement,  in  which 
the  sensory  loss  is  frequently  on  the  same  side  as  the 
lesion.  The  explanation  of  this  is  that  in  such  cases  the 
sensory  path  is  involved  (in  its  ascent)  before  it  crosses  to 
the  opposite  side. 


FIG.    72. 

Areas  of  ansesthesia 
and  hypersesthesia  in 
case  of  Brown-S6quard 
paralysis.  Lines  indi- 
cate ansesthesia  ;  dots 
indicate  hyperaesthe- 
sia.    (Starr.) 


FIG.    73. 


Diagram   of   area  of  sensory  loss  in  case  of 
crush  of  first  lumbar  segment  of  cord. 


In  unilateral  cord  lesions  the  muscular  sense  may  be 
impaired  or  lost  in  the  muscles  below  the  level  of  the 
lesion,  but  it  is  impaired  on  the  same  side  as  the  lesion, 
since,  as  already  stated  (p.  134),  the  path  for  the  muscular 
sense  does  not  cross  in  the  cord.  Of  the  other  forms  of 
sensibility  those  for  pain  and  temperature  are  almost 
constantly  impaired,  and  in  the  majority  of  cases  tactile 


DIAGNOSIS  OF  THE  POSITION  OF  THE  LESION.       261 

sensibility  is  also  affected.  There  is  often  an  area  of 
hyperalgesia  on  the  side  of  the  lesion  which  corresponds 
in  position  with  the  anaesthesia  of  the  opposite  side.  The 
reflexes,  superficial  and  deep,  are  increased  below  the 
lesion  on  the  same  side,  except  at  the  onset  of  acute 
lesions,  when  there  is  sometimes  loss  of  knee-jerk  on  the 
same  side. 

Besides  these  motor  and  sensory  phenomena  below  the 
level  of  the  lesion  there  are  others  at  the  same  level  and  on 
the  same  side.  There  are  (a)  a  zone  of  hyperalgesia  due 
to  irritation  of  sensory  nerve-roots  at  the  upper  level  of 
the  lesion  ;  (^)  a  narrow  zone  of  anaesthesia  just  below 
(«),  from  injury  to  the  sensory  roots  before  they  cross  ; 
and  {c)  localized  unilateral  degenerative  muscular  atrophy 
in  cases  where  a  considerable  number  of  motor  cells  are 
damaged.  The  effects  of  this  damage  are  best  observed  in 
lesions  of  the  cervical  or  lumbar  enlargement. 

The  typical  results  of  a  unilateral  lesion  '  of  the  cord 
may  conveniently  be  tabulated  as  follows  : 

A.  At  or  near  the  level  of  the  lesion  and  on  the  same 

side  of  the  body — 

A  band  of  hyperalgesia. 
A  band  of  anaesthesia. 

B.  Below  the  level  of  the  lesion  and  on  the  same  side — • 

Motor  paralysis. 

Hyperalgesia. 

Impairment  or  loss  of  muscular  sense  (sometimes 

with  ataxia). 
Early  loss  of  reflexes,  including  knee-jerk  (in 

acute  cases). 
Subsequent  increase  of  knee-jerk  and  frequently 

ankle-clonus. 

*  This  characteristic  group  of  motor  and  sensory  symptoms  is  some- 
times denominated  Brown-Sequard's  paralysis. 


262        DISEASES   OF  THE   NERVOUS   SYSTEM. 

Temperature  raised.  Often  the  side  below  the 
lesion  is,  for  the  first  few  days  or  weeks, 
warmer  than  the  other,  the  difference  being 
usually  about  a  degree  Fahrenheit.  This 
difference  usually  disappears  in  time,  to  be 
replaced  by  the  reverse,  the  side  below  the 
lesion  being  colder. 
C.  Below  the  level  of  the  lesion  and  on  the  opposite 
side — 

Loss  of  sensation  (pain,  temperature,  touch). 
Temperature  same  as  that  above  lesion. 
A  Complete  Transverse  Lesion  of  the  cord  gives  rise  to 
loss  of  motor  power  and  loss  of  all  varieties  of  sensibility 
below  the  level  of  the  lesion.  The  motor  and  sensory  loss 
is  as  complete  (so  far  as  voluntary  motion  and  sensation 
are  concerned)  as  though  the  entire  cord  below  the  lesion 
were  destroyed,  since  motor  and  sensory  conduction  are 
abolished.  In  other  words,  the  functions  of  the  cord  as 
a  conductor  to  and  from  the  brain  are  destroyed  as  re- 
gards parts  below  the  level  of  the  disease.  It  is  otherwise 
with  the  functions  of  the  cord  as  a  centre — that  is,  as  a 
trophic  and  reflex  centre.  The  ganglion-cells  of  the 
anterior  horns,  being  intact  below  the  lower  level  of  the 
morbid  process,  still  continue  to  subserve  their  trophic 
and  reflex  functions.  Hence  there  is  no  degenerative 
atrophy  in  the  muscles  supplied  by  nerves  derived  from 
the  part  of  the  cord  below  the  lesion.  The  ganglion- 
cells  that  subserve  the  various  reflexes,  being  no  longer 
under  cerebral  control,  overact,  and  this  overaction  is 
shown  by  increased  knee-jerks  and  often  by  the  existence 
of  ankle-clonus.  It  must  be  remembered,  however,  that 
the  knee-jerks  may  be  abolished  for  days  or  weeks  in 
consequence  of  inhibition  from  the  irritation  of  the 
lesion.     In   such   cases  overaction   eventually  sets  in,  if 


DIAGNOSIS  OF  THE  POSITION  OF  THE  LESION.       263 

the  patient  survives  the  damage  to  the  cord  sufficiently 
long. 

In  addition  to  these  phenomena  dependent  on  a  com- 
plete transverse  lesion  of  the  cord,  there  may  be  after  a 
time  degenerative  atrophy  in  certain  groups  of  muscles 
corresp072ding  to  the  level  of  the  lesion.  This  atrophy  de- 
pends on  the  destruction  of  ganglion-cells  of  the  anterior 
cornua  at  the  level  of  the  lesion;  hence  when  the  lesion 
is  of  slight  vertical  extent  the  atrophy  may  be  impercep- 
tible, but  when  the  lesion  is  of  considerable  vertical 
extent  the  atrophy  has  a  correspondingly  wide  distribu- 
tion. The  atrophy  is  of  course  chiefly  noticeable  when 
the  disease  is  in  the  cervical  and  lumbar  enlargements. 
Just  above  the  level  of  the  anaesthesia  there  is  usually 
a  girdle  pain  or  a  band  of  hyperalgesia.  This  depends 
on  sensory  irritation  in  the  lower  end  of  the  upper 
portion  of  the  normal  cord. 

We  may  tabulate  the  results  of  a  complete  transverse 
lesion  as  follows  : 

A.  At  the  level  of  the  lesion — 

A  zone  of  hypersesthesia. 

Muscular  atrophy  of  limited  distribution. 

B.  Below  the  level  of  the  lesion — 

Complete  motor  paralysis. 

Complete  sensory  paralysis  (all  forms). 

Initial  loss  of  knee-jerk  (in  acute  lesions). 

Eventual  excess  of  knee-jerk  and  ankle  clonus. 
The  distribution  of  these  symptoms  vertically  depends 
on  the  level  of  the  cord  at  which  the  lesion  is  situated, 
and  this  is  true  also  of  unilateral  lesions  of  the  cord. 
In  every  case  it  is  necessary  to  determine  as  accurately 
as  possible  the  upper  and  lower  limits  of  the  lesion. 
The  upper  limit  of  the  lesion  is  indicated  by  the  upper 
limit  of  the  anaesthesia  and  motor  paralysis.     More  than 


264 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


this  cannot  be  learned  from  the  distribution  of  the  motor 
and  sensory  paralysis,  since  this  is  the  same  whatever 
may  be  the  downward  extent  of  the  lesion.  In  order  to 
determine  the  lower  level  of  the  lesion  it  is  necessary  to 
study  the  condition  of  the  reflexes  and  the  trophic  state 

of  the  muscles — that  is,  to  interro- 
gate the  cord  as  a  central  organ. 
If  reflex  action  is  retained,  this 
shows  that  the  reflex  or  loops 
on  which  the  reflexes  depend  are 
not  included  in  the  lesion.  On 
the  other  hand,  loss  of  reflex  action 
indicates  that  the  lesion  has  de- 
stroyed the  integrity  of  the  reflex 
loops,  and  presumably  that  of  the 
ganglion-cells,  or  nerve-roots,  or 
both,  on  which  the  reflex  depends. 
Both  the  deep  and  superficial  re- 
flexes should  be  studied  with  care. 
The  table  on  page  2^  shows  the 
regions  of  the  cord  with  which  the 
different  reflexes  are  in  relation, 
and  with  this  knowledge  it  is  easy 
to  infer  from  the  state  of  the  re- 
se?so?y'"iSsi??rse"?fc'l-u\\of  ^  whcthcr   particular  regions 

'i^:'^SSlu^Tl:lS^.  of  the  cord  have  retained  or  lost 

and  anaesthesia  in  the  arms  is   fl-,p|».  intPCTritv 
characteristicof  a  lesion  at  this    l-"^''    llUCj^lliy. 

doued.  ^'^^  °^  hyperalgesia      ^^c  extent   downwards  of   the 

lesion  is  indicated  also  by  the  state 
of  muscular  nutrition  and  the  electrical  reactions.  The 
presence  of  atrophy  and  of  R  D  shows  that  the  anterior 
cornua  or  the  corresponding  motor  roots  have  been 
damaged,  and  the  extent  of  these  changes  indicates  the 
precise  levels  thus  affected.  In  order  to  localize  accu- 
rately the  lower  level  of  the  lesion  by  inference  from  the 


FIG.  74. 


DIAGNOSIS  OF  THE  POSITION  OF  THE   LESION.     265 

trophic  state,  it  is  necessary  to  bear  in  mind  the  relations 
of  the  various  muscles  and  muscle-groups  to  the  cord. 
These  relations  are  given  in  the  table.  The  indications 
of  the  extent  of  the  lesion  afforded  by  the  trophic  state 
of  the  muscles  are  especially  valuable  when  the  disease 
is  in  the  lumbar  and  cervical  enlargements.  When  the 
destructive  process  is  in  the  dorsal  region  the  effect  on 
muscular  nutrition  is  less  noticeable  and  less  valuable  as 
an  aid  in  localizing  the  lesion,  but  it  is  just  in  this  re- 
gion that  the  indications  obtained  from  the  state  of  the 
reflexes  are  of  the  greatest  aid. 

With  the  help  of  these  facts,  and  the  tables  showing 
the  representations  of  the  motor,  sensory,  and  reflex 
functions  of  the  cord,  it  is  possible,  in  most  cases,  to 
make  an  accurate  diagnosis  of  the  position  and  extent 
of  the  lesion.  It  may  be  well,  however,  to  outline 
briefly  the  distribution  of  the  motor  and  sensory  loss 
that  results  from  a  complete  transverse  lesion  of  the  cord 
at  the  most  important  levels  of  the  cord.  Individual 
differences  exist  in  the  distribution  of  symptoms  from 
disease  at  the  same  levels,  but  these  differences  are  sel- 
dom considerable,  and  do  not  seriously  invalidate  the 
following  types. 

A  lesion  which  destroys  only  the  extremity  of  the  cord 
(conus  medullaris)  as  high  as  the  fifth  sacral  nerves, 
causes  paralysis  of  the  bladder  and  rectum,  and  a  small 
area  of  anaesthesia  near  the  tip  of  the  coccyx.  Such 
lesions  are  very  rare.  If  the  lesion  destroys  the  cord  at 
the  level  of  the  fourth  and  fifth  sacral  segments  there 
is,  besides  paralysis  of  bladder  and  rectum,  loss  of  power 
in  the  perineal  muscles  (erector  penis,  transversus  peri- 
nei,  accelerator  urinae),  with  loss  of  ejaculatory  and  erec- 
tile power.  There  is  also  a  characteristic  anaesthetic  area, 
which  probably  depends  on  injury  of  the  fourth  sacral 
segments  or  roots.     There   is  a  saddle-shaped  region  of 


266         DISEASES   OF  THE   NERVOUS   SYSTEM. 

anaesthesia  on  the  back  of  the  thighs  and  sacrum.  The 
internal  surfaces  of  the  thighs  high  up  are  also  anaes- 
thetic, and  the  ansesthesia  usually  extends  to  the  exter- 
nal genitals  and  perineum.  Figure  75  represents  the 
saddle-shaped  area  in  such  a  case. 

In  lesions  involving  the  upper  sacral  segments  there  is 
paralysis  of  the  muscles  of  the  leg  and  foot,  and  a  strip  of 
anaesthesia  on  the  back  of  the  thigh,  which  extends  to  the 
back  of  the  leg  and  ankle  and  to  the  sole  and  dorsum  of 
the  foot.  The  skin  of  the  inner  side  of  the  leg  usually 
escapes. 

Damage  to  the  cord  as  high  as  the  lumbar  region 
causes  paralysis  of  the  flexors  of  the  knee  and  abductors 
of  the  thigh.  There  is  also  anaesthesia  of  the  anterior  and 
inner  aspect  of  the  leg  and  of  the  inner  and  posterior  part 
of  the  thigh. 

When  the  middle  of  the  lumbar  region  is  destroyed,  the 
motor  paralysis  includes  the  extensors  of  the  knee  and  the 
abductors  of  the  thigh,  and  the  loss  of  sensation  extends 
as  high  as  the  anterior  aspect  of  the  thigh  (lower  part  at 
least).  When  the  disease  affects  the  upper  part  of  the 
lumbar  enlargement  the  loss  of  sensibility  includes  the 
upper  and  outer  aspect  of  the  thigh  and  the  skin  of  the 
groin  and  part  of  the  scrotum.  The  flexors  of  the  thigh 
and  the  sartorius  are  then  paralyzed. 

As  the  level  of  the  lesion  ascends  in  the  dorsal  region 
the  level  of  the  anaesthesia  and  motor  paralysis  extends  to 
a  correspondingly  higher  level  on  the  trunk.  The  ab- 
dominal muscles  are  first  paralyzed,  then  the  intercostals. 
The  umbilicus  corresponds  to  the  tenth  dorsal  nerves. 
When  the  anaesthesia  reaches  one  inch  above  the  um- 
bilicus the  lesion  is  as  high  as  the  ninth  dorsal  nerves. 
The  epigastrium  corresponds  to  the  sixth  and  seventh 
dorsal  segments,  the  nipples  to  the  fourth  dorsal,  and 
the  third  rib  to  the  third  dorsal  segment. 


DIAGNOSIS  OF  THE  POSITION  OF  THE  LESION.       267 

When  a  lesion  is  placed  as  high  as  the  first  dorsal 
segment  (that  is,  the  lower  part  of  the  cervical  enlarge- 
ment) the  first  impairment  of  sensibility  and  loss  of  power 
in  the  upper  extremity  are  observed.  There  is  loss  of 
power  in  the  intrinsic  muscles  of  the  hand  and  loss  of 
sensibility  in  part  or  all  of  the  area  of  the  hand  supplied 
by  the  ulnar  nerve.  When  the  lesion  invades  the  cord  at 
the  level  of  the  seventh  cervical  segment  the  anaesthesia 
usually  reaches  as  high  as  the  median  line,  anteriorly  and 
posteriorly,  of  the  arm,  forearm,  and  hand.  Figure  50 
shows  this  characteristic  distribution  of  anaesthesia  in 
a  case  of  total  transverse  lesion  at  this  level  of  the  cord. 
The  motor  loss  in  such  cases  is  sufficiently  indicated  by 
the  table. 

A  lesion  destroying  the  middle  of  the  cervical  enlarge- 
ment (fifth,  sixth,  seventh)  causes  loss  of  sensation  in  the 
entire  arm  and  part  of  the  shoulder.  The  motor  paralysis 
extends  to  the  shoulder  muscles  and  the  serratus  magnus. 
There  is  also  sometimes  some  loss  of  power  in  the  tra- 
pezius and  sterno-mastoid  when  the  lesion  is  placed  as 
high  as  the  fifth  cervical  segment.  When  the  fourth 
cervical  segment  is  destroyed  the  anaesthesia  extends  to 
the  entire  shoulder  and  lower  part  of  the  neck.  The 
action  of  the  diaphragm  is  impaired  and  the  motor  paral- 
ysis extends  to  the  few  remaining  muscles  of  the  shoulder 
(supra-  and  infra-spinati).  A  complete  transverse  lesion 
at  this  level  is  usually  quickly  fatal.  The  accessory  mus- 
cles of  respiration  (scaleni,  sterno-mastoids)  may  give  the 
patient  enough  air  to  maintain  life  a  few  days,  but  not 
longer.  In  the  lower  part  of  the  cervical  cord  an  acute 
lesion  may  inhibit  respiration  so  as  to  cause  death  in  the 
course  of  a  few  days. 

Nerve-Roots. — Lesions  of  the  Anterior  Nerve-Roots 
give  rise  to  motor  over-action  or  motor  paralysis  accord- 
ing as  they  are  irritative  or  destructive  in  character.    The 


268        DISEASES   OF  THE   NERVOUS   SYSTEM. 

distribution  of  the  spasm  and  paralysis  depends  on  the 
number  and  locality  of  the  roots  involved.  The  table 
(on  page  23)  shows  the  representation  of  the  different 
muscles  in  the  anterior  roots,  this  being  practically  the 
same  as  in  the  corresponding  segments  of  the  cord.  In 
chronic  irritative  disease  long-continued  and  persistent 
spasm  (from  tumor)  may  produce  loss  of  voluntary 
power,  and  in  acute  irritative  lesions  (meningitis)  irri- 
tation symptoms  far  exceed  paralytic  phenomena  and 
may  even  exist  alone. 

Irritative  lesions  of  the  Posterior  Nerve- Roots  cause  pain 
and  hyperalgesic  skin  areas  corresponding  to  the  irritated 
roots.  The  pain  is  often  severe  and  persistent.  Destruc- 
tive lesions  cause  loss  of  sensibility.  When  the  destruc- 
tion is  partial,  tactile  sensibility  may  be  chiefly  impaired  ; 
when  it  is  complete,  all  forms  of  sensibility  are  abolished 
in  the  corresponding  skin  area. 

Cauda  Equina. — The  cauda  equina  not  very  in- 
frequently suffers  from  the  effects  of  pressure.  This 
pressure  is  exerted  most  often  in  consequence  of  injury 
to  the  lumbar  spine,  especially  dislocation.  Less  fre- 
quently the  pressure  results  from  tumor  or  from  spina 
bifida.  The  resulting  symptoms  vary  considerably  ac- 
cording to  the  position  and  extent  of  the  lesion.  In 
a  lesion  which  involves  the  entire  cauda  equina,  or  the 
larger  number  of  its  constituent  roots,  the  nerve-roots 
which  take  their  origin  from  the  lowest  part  of  the  cord 
(that  is,  lie  nearest  the  median  line)  are  more  seriously 
injured  than  those  above  them.  If  all  the  roots  are  origi- 
nally involved  the  upper  ones  may  soon  recover  entirely, 
while  the  lower  ones  continue  to  suffer  seriously.  This  is 
a  fact  of  some  diagnostic  importance.  While  there  is 
nothing  absolutely  distinctive  about  the  distribution  of 
the  motor  and  sensory  symptoms  in  cases  of  injury  to  the 
cauda   equina,  there   is    considerable   uniformity  in    the 


DIAGNOSIS  OF  THE  POSITION  OF  THE  LESION.       269 

phenomena,  and  many  of  the  cases  conform  more  or  less 
closely  to  a  certain  type.  The  motor  paralysis  is  espe- 
cially apt  to  affect  the  branches  of  the  sciatic  and  pudic 
nerves,  and  particularly  the  lower  branches  of  the  former. 
The  anterior  crural  and  obturator  distribution  are  also 
frequently  involved,  but  the  paralysis  is  apt  to  be  less  in 
degree.  The  R  D  may  or  may  not  be  present,  according 
to  the  severity  of  the  damage.  The  anaesthesia  com- 
monly involves  especially  the  distribution  of  the  great 
and  small  sciatic  and  pudic  nerves.  When  the  fourth  and 
fifth  sacral  roots  suffer  chiefly,  as  they  sometimes  do^  the 
anaesthesia  is  limited  to  the  perineum,  external  genitals, 
and  a  saddle-shaped  area  on  the  buttocks  and  thighs. 
Sometimes  the  anaesthesia  is  limited  to  the  perineum  and 
genitals  and  upper  part  of  the  inner  surfaces  of  the  thighs, 
even  though  there  is  considerable  loss  of  power  in  the 
lower  extremities. 

The  condition  of  the  reflexes  is  different  in  different 
cases.  The  knee-jerk  is  usually  absent,  as  is  also  the 
plantar  reflex.  Retention  of  urine,  with  overflow  incon- 
tinence, is  not  common.  Such  incontinence  may  exist 
for  several  months  in  consequence  of  a  cauda  injury,  and 
yet  terminate  in  recovery  of  function  when  the  pressure 
ceases  or  diminishes.  As  a  rule,  the  sphincters  are  only 
slightly  or  not  at  all  affected  in  pure  cauda  lesions. 
Trophic  disturbances  (bed-sores,  perforating  ulcer)  occur 
in  a  considerable  proportion  of  cases.  The  distinction  of 
cauda  equina  disease  from  lesions  of  the  lower  part  of  the 
spinal  cord  may  be  exceedingly  difficult.  If  the  damage 
is  of  traumatic  origin  the  position  of  the  local  symptoms 
(fracture,  displacement  of  vertebrae,  etc.)  is  of  much 
assistance,  since  the  cord  itself  does  not  extend  below 
the  lower  border  of  the  first  lumbar  vertebra,  and  any 
displacement  below  this  level  would  injure  the  cauda  and 
not  the  cord.     In  the  absence  of  distinct  local  indica- 


270        DISEASES   OF   THE   NERVOUS    SYSTEM. 

tions,  the  distribution  of  the  motor  and  sensory  phe- 
nomena and  their  mode  of  development  may  be  of  aid. 
Anaesthesia  limited  to  the  buttocks  (saddle-shaped  areas) 
or  to  the  buttock  and  backs  of  the  thighs,  or  to  the  but- 
tocks and  thighs  and  the  legs  (posterior  aspect),  suggests 
a  dependence  on  a  cauda  lesion  and  not  on  a  cord  lesion, 
but  it  is  not  certain  that  anaesthesia  of  similar  distribu- 
tion may  not  result  from  partial  destruction  of  the  conus 


Area  of  anaesthesia 
in  a  lesion  of  the 
Cauda  equina,  depen- 
dent probably  on 
damage  to  the  fourth 
and  fifth  sacral  roots. 
(Starr.) 


FIG.    76. 

Diagram  showing  the  area  of  anaesthe- 
sia in  a  woman  with  a  lesion  of  the  cauda 
equina. 


medullaris  and  lumbar  cord  in  cases  where  there  is  little 
or  no  involvement  of  the  nerve-roots.  Considerable  sen- 
sory loss  (as  that  shown  in  diagram  75),  with  slight  loss  of 
motor  power  and  slight  involvement  of  the  sphincters,  also 
suggests  a  cauda  and  not  a  cord  lesion.  Pain  in  the  area 
of  anaesthesia  points  to  a  cauda-equina  lesion,  pain  above 
the  area  of  anaesthesia  to  a   cord   lesion.     The  pain  of 


DIAGNOSIS  OF  THE   POSITION  OF  THE  LESION.      271 

Cauda  lesions  is  referred  to  the  sacrum  rather  than  the 
lumbar  spine,  which  is  generally  the  seat  of  pain  in 
spinal-cord  disease.  With  the  aid  of  these  points  of  dis- 
tinction a  diagnosis  can  generally  be  made  between 
damage  of  the  lumbar,  or  lumbar  and  sacral  cord,  and 
damage  of  the  cauda  equina.  But  when,  as  is  probably 
not  rarely  the  case,  the  conus  medullaris  is  involved 
with  the  Cauda  equina,  the  recognition  of  this  involve- 
ment may  be  impossible.  As  already  stated,  it  is  not 
certain  that  damage  of  the  conus  and  lower  end  of  the 
cord  may  not  be  competent  to  cause  some  of  the  pecul- 
iarly disposed  anaesthesias  which  are  thought  to  be 
characteristic  of  a  cauda  lesion.*  It  may  be  that  the 
involvement  of  the  conus  simply  intensifies  the  symptoms 
of  cauda  disease.  Destruction  of  the  conus  medullaris 
causes  complete  paralysis  of  the  bladder  and  rectal 
sphincters  and  loss  of  sexual  power.  It  is  not  yet  known 
whether  such  complete  paralysis  is  ever  the  result  of 
pure  lesions  of  the  cauda.  There  is  some  reason  to  think 
it  is  not.  When,  therefore,  the  symptoms  suggest  a  cauda 
lesion,  but  the  sphincters  are  completely  paralyzed,  there 
is  reason  to  think  that  the  conus  medullaris  is  also  im- 
plicated. Further  investigation  is  needed  to  clear  up 
these  points.  Asymmetry  of  the  motor  and  sensory  loss 
suggests  a  lesion  of  the  cauda  rather  than  of  the  cord, 
and  extreme  chronicity  of  development  (years)  has  the 
same  significance. 

*  Thus  in  one  case  of  dislocation  of  the  first  lumbar  vertebra  there 
was  complete  paralysis  of  motion  below  the  knee  and  anaesthesia  of 
the  buttock,  back  of  thigh,  leg,  and  sole  of  foot,  but  the  autopsy 
failed  to  show  any  damage  to  the  cauda  equina.  The  autopsy  did 
show,  however,  crushing  of  the  sacral  and  lowest  lumbar  segments  of 
the  cord  and  slight  damage  of  the  nerve-roots  as  they  lie  on  the  cord 
at  this  level. 


2/2         DISEASES   OF   THE   NERVOUS   SYSTEM. 


The     distinction      of      disease      or      injury     of     the 
Cauda  equina    from     lesions    of    the    peripheral   nerves 


is  usually  not  difficult, 
only  disease  of  the 
peripheral  nerves  that 
can  be  mistaken  for  a 
Cauda  lesion.  The  diag- 
nostic points  are  else- 
where presented  (p.  538) 
Occasionally  an  injury 
of  the  nerves  in  their 
extra-spinal  course,  par- 
ticularly one  involving 
the  lumbo- sacral  plexus, 
gives  rise  to  considerable 
diagnostic  difficulty.  The 
points  to  be  borne  in 
mind  in  making  the  dis- 
tinction are  the  bilateral 
symmetry  (not  always 
perfect)  of  the  symptoms 
from  Cauda  injury,  and 
the  usual  occurrence  of 
local  evidences  of  injury. 
In  rare  instances  injuries 
of  the  Cauda  have  pro- 
duced   chiefly    unilateral 


Multiple     neuritis    is    the 


FIG.  77. 


motor    and    sensory  SVmp-  .    Diagram  showing  the  area  of  sensory  loss 

''       •'       ^      in  a  case  of  crush  of  the  cauda  equina  and 

tOmS,     but     even    in     these  co""s  medullarisa,  .r,  area  of  anesthesia 

'  and  analgesia.      1  he   lightly    shaded  areas 

cases      there      are      usually  o"  '^^  buttocks  and  legs  represent  a  slight- 

•^    er  degree  of  sensory  loss. 

some       symptoms       that 

suggest    an    intra-spinal    nerve    lesion    (disturbances   of 

bladder  and  rectum,  peculiar  distribution  of  anaesthesia, 

etc.). 


DIAGNOSIS  OF  THE  POSITION  OF  THE  LESION.      273 

Peripheral  Nerves. — The  localization  of  lesions  in- 
volving the  nerves  in  their  extra-cranial  and  extra-spinal 
course  is,  generally  speaking,  less  difficult  than  the  locali- 
zation of  lesions  of  the  brain  and  spinal  cord.  The  data 
for  an  accurate  local  diagnosis  are  easier  to  obtain  and 
are  less  equivocal  in  significance  than  in  the  case  of  cen- 
tral lesions  ;  local  signs  play  a  more  important  role  and 
the  diagnosis  is  less  distinctly  inferential  in  character. 
An  accurate  knowledge  of  the  course  and  distribution 
of  the  nerves  and  of  the  anomalies  that  occur,  must  be 
the  foundation  on  which  every  diagnosis  rests.  The  pos- 
sibilities of  collateral  innervation  must  also  be  borne  in 
mind  in  determining  the  effect  of  a  lesion  in  a  given 
situation. 

The  general  symptomatic  characters  of  peripheral- 
nerve  lesions  may  conveniently  be  considered  in  the  chap- 
ter on  clinical  types.  The  special  symptomatic  charac- 
ters of  such  lesions  vary  with  the  special  functions  and 
distributions  of  the  nerve  or  nerves  implicated.  Certain 
symptomatic  combinations  are  sufficiently  frequent  and 
important   to  require  special  notice,  and  are  mentioned 

as  clinical  types  of  disease. 
18 


CHAPTER  IV. 

THE    DIAGNOSIS    OF    THE    NATURE    OF    THE    LESION. 

Having  established  the  situation  of  the  lesion  in  a 
given  case  of  organic  disease  of  the  nervous  system,  there 
remains  for  determination  the  nature  of  the  morbid  pro- 
cess which  constitutes  the  lesion.  Generally  speaking, 
this  problem  presents  greater  difficulties  than  the  local 
diagnosis.  In  many  instances,  it  is  true,  an  exact  diag- 
nosis of  the  nature  of  the  lesion  is  readily  reached,  but 
the  cases  are  quite  as  numerous  in  which  an  approximate 
diagnosis  only  can  be  made.  Sometimes  the  best  that 
can  be  done  is  to  narrow  the  diagnosis  to  one  of  two 
possibilities,  and  occasionally  it  is  impossible  to  do  better 
than  to  make  a  guess. 

Notwithstanding  the  obstacles  to  an  exact  diagnosis  of 
the  character  of  the  pathological  process,  the  problem  is 
one  of  the  highest  practical  importance,  and  demands  for 
its  solution  the  most  painstaking  care  in  balancing  the 
available  diagnostic  indications.  In  the  case  of  lesions  of 
the  central  nervous  system  the  pathological  diagnosis  is 
usually  of  distinctly  greater  importance  to  the  patient 
than  the  exact  local  diagnosis,  for  on  it  depends,  in  great 
degree,  both  the  prognosis  and  the  treatment. 

Before  studying  the  more  important  indications  that 
guide  us  in  determining  the  nature  of  the  lesion  it  is  use- 
ful to  consider  briefly  the  various  morbid  processes  which 
are  encountered  in  practice  and  constitute  the  great 
17  274 


DIAGNOSIS   OF   THE  NATURE   OF   THE   LESION.     275 

majority  of  the  cases  of  nervous  disease.  These  processes 
are  few  if  we  consider  only  the  ultimate  processes  to 
which  the  symptoms  of  disease  are  due.  They  are  hem- 
orrhage, necrotic  softening,  inflammation,  abscess,  tumor, 
and  degeneration.  To  this  list  may  conveniently  be 
added  congestion  and  anaemia,  although  these  are  not, 
strictly  speaking,  organic  conditions. 

Hyperaemia. — The  subject  of  Congestion  of  the  Brain 
is  one  of  considerable  obscurity.  It  cannot  be  said  that 
we  possess  any  exact  knowledge  in  regard  to  it. 

The  results  of  post-mortem  examination  are  to  a  con- 
siderable extent  negative — that  is,  there  are  no  constant 
or  characteristic  changes  in  cases  which,  from  their  symp- 
toms, seem  referable  to  cerebral  congestion.  This  fact, 
however,  does  not  in  itself  make  the  possibility  of  the  oc- 
currence of  congestion  impossible,  since  general  pathology 
teaches  that  distinct  active  congestion  of  other  parts  may 
leave  no  trace  after  death.  Indeed  cases  occasionally 
occur  in  which  the  symptoms  can  reasonably  be  referred 
to  cerebral  congestion  alone.  The  hypersemia  may  be 
active  or  passsive.  In  the  former  case  there  is  an  excess 
of  blood  in  the  arteries,  in  the  latter  an  excess  in  the 
veins.  In  both  instances  the  capillaries  are  over-distended, 
and  it  is  to  this  over-distension  that  the  symptoms  of  con- 
gestion are  due.  In  both  instances  the  brain  suffers  from 
a  deficiency  of  oxygen,  in  consequence  of  the  stasis,  but 
in  passive  congestion  there  is  also  an  excessive  accumula- 
tion of  carbonic  acid  in  the  capillaries.  It  is  probable 
that  prolonged  passive  congestion  during  life  may  cause  a 
permanent  increase  in  the  size  of  the  capillaries.  Me- 
chanical venous  congestion  may  result  a  short  time  after 
death  from  gravitation  of  blood  to  dependent  portions  of 
the  brain.  When  ante-mortem  passive  congestion  has  ex- 
isted in  such  cases,  its  effects  cannot  be  distinguished  in 


2/6         DISEASES   OF   THE   NERVOUS    SYSTEM. 

the  presence  of  the  more  obtrusive  results  of  gravitation. 
It  is  important  to  note  that  even  the  most  intense  passive 
congestion,  such  as  occurs  in  asphyxia,  may  leave  no 
trace  after  death. 

What  has  been  said  of  our  imperfect  knowledge  of  cer- 
ebral congestion  may  be  said  with  equal  truth  of  congestion 
of  the  cord.  It  is  probable  that  active  primary  congestion 
of  the  cord  occurring  independently  of  the  initial  stage 
of  myelitis  is  an  exceedingly  rare  condition.  A  so-called 
secondary  congestion  of  the  cord  is  not  an  infrequent 
consequence  of  excessive  physiological  activity  of  the 
nerve  elements  of  the  cord,  especially  of  the  motor 
elements.  Passive  congestion  of  the  cord  is  of  exceed- 
ingly rare  occurrence.  The  influence  of  gravitation  in 
producing  mechanical  congestion  of  the  cord  after  death 
is  probably  as  great  as  in  the  case  of  the  brain.  The  same 
influence  is  operative  in  the  cord  during  life,  but  to  a  far 
slighter  degree. 

Of  congestion  of  the  membranes  of  the  brain  and  spinal 
cord,  as  conditions  distinct  from  the  first  stage  of  inflam- 
mation, nothing  is  known.  Likewise  nothing  is  known  of 
simple  congestion  of  the  peripheral  nerves. 

Anaemia. — Ancemia  of  the  Brain  may  result  from  gen- 
eral anaemia,  in  which  the  quantity  or  quality  of  the  entire 
amount  of  blood  is  defective.  This  is  seen  in  cases  of 
simple  anaemia,  hemorrhage,  chlorosis,  etc.  The  blood 
supplied  to  the  brain  may  also  be  diminished  in  the 
absence  of  any  systemic  causes  for  such  diminution,  as 
from  cardiac  weakness.  Localized  cerebral  anaemia  may 
result  from  obstruction  to  the  flow  of  blood  through  the 
cerebral  vessels.  Permanent  obstruction  of  this  kind 
often  leads  to  another  pathological  process — that  is, 
softening.  The  various  causes  of  anaemia  of  the  brain 
may  be  suddenly  or  gradually  operative,  and  the  symp- 


DIAGNOSIS   OF   THE   NATURE   OF   THE    LESION.     277 

toms  vary  accordingly.  There  is  some  reason  for  be- 
lieving that  angiospasm  (arterial  spasm)  is  capable  of 
causing  ansemia  of  greater  or  less  areas  of  brain  sub- 
stance, sometimes  with  resulting  temporary  hemiplegia 
symptoms. 

AncBmia  of  the  Spinal  Cord,  as  a  persistent  condition, 
dependent  on  arterial  obstruction,  is  unknown,  but  it  is 
certain  that  such  mechanical  obstruction  to  the  blood- 
supply  of  the  cord  may  result  in  local  anaemic  necrosis 
and  subsequent  inflammation.  It  is  uncertain  whether 
the  symptoms  that  suggest  transient  ansemia  of  the  cord 
depend  primarily  on  arterial  spasm,  or  are  due  to  primary 
functional  derangement  of  the  nerve  elements,  causing 
arterio-spasm.  In  certain  blood  states,  as  simple  anaemia, 
chlorosis,  and  anaemia  from  blood  loss,  the  nutrition  of 
the  entire  body  suffers,  and  with  this  the  nutrition  and 
functional  activity  of  the  spinal  cord.  Here,  as  in  the 
brain,  the  essential  pathological  factor  is  the  defective 
quantity  or  quality  of  the  blood.  Concerning  anaemia  of 
the  peripheral  nerves  nothing  is  known. 

Hemorrhage. — Hemorrhage  within  the  Cranial  Cavity 
may  invade  the  brain  substance  itself  or  the  meninges. 
In  either  case  the  hemorrhage  is  due  to  rupture  of  a  ves- 
sel. Meningeal  hemorrhage  is  almost  invariably  ^  due  to 
injury  ;  hemorrhage  into  the  substance  of  the  brain  (in- 
cluding pons,  medulla,  and  cerebellum)  generally  occurs 
spontaneously— that  is,  as  the  result  exclusively  of  in- 
ternal pathological  conditions.  The  hemorrhage  is  usu- 
ally from  an  artery.  But  occasionally  it  is  from  a  vein  or 
from  capillaries.  Excepting  from  traumatic  influences, 
an  artery  ruptures  only  when  its  walls  are  the  seat  of 
disease.     The  local  factor  in  producing  hemorrhage  may 

^  In  children  extensive  subarachnoid  hemorrhage  sometimes  occurs 
in  the  course  of  acute  infectious  diseases. 


2/8         DISEASES   OF   THE   NERVOUS   SYSTEM. 

be  the  sole  appreciable  cause  of  the  rupture.  Frequently, 
however,  there  is  a  local  increase  in  blood  pressure,  and 
such  an  increase  causes  the  diseased  and  weakened 
arterial  wall  to  give  way  more  readily  than  it  would 
otherwise  do. 

When  the  walls  of  an  artery  become  weakened  by  dis- 
ease they  gradually  yield  before  the  blood  pressure.  This 
gradual  yielding  leads  to  local  thinning  of  the  coats  of 
the  vessel,  which  eventually  become  so  thin  and  weak  that 
they  may  rupture.  As  the  walls  yield  before  the  pressure 
of  blood,  a  bulging  occurs,  and  this  bulging  constitutes  an 
aneurism.  Aneurisms  occur  in  two  different  situations — 
in  the  larger  arteries  at  the  base  of  the  brain  and  over  the 
convexity,  and  in  the  small  arteries  that  lie  imbedded 
within  the  brain  substance.  Aneurisms  of  the  former 
class  are  of  uncommon  occurrence.  They  usually  attain 
considerable  size  and  are  few  in  number  or  single.  They 
may  give  rise  to  symptoms  due  to  pressure,  and  this  is 
especially  liable  to  occur  when  they  are  situated  on  ves- 
sels at  the  base  of  the  brain.  These  aneurisms  (intra- 
cranial aneurism  proper)  may  eventually  rupture,  but, 
until  they  do  so,  their  symptoms,  if  symptoms  exist,  are 
those  of  intracranial  tumor.  The  aneurisms  within  the 
substance  of  the  brain,  which  form  on  the  small  arterial 
branches,  are  of  small  size  d^-ji  to  -^q  inch)  and  are 
hence  termed  miliary  aneurisms.  These  miliary  aneu- 
risms are  always  numerous.  They  are  found  most  fre- 
quently on  the  vessels  to  the  central  ganglia,  probably 
because  these  small  vessels  are  given  off  directly  from  a 
vessel  (middle  cerebral)  of  much  greater  calibre,  in  con- 
sequence of  which  the  arterial  pressure  is  considerably 
higher  in  them  than  in  vessels  of  the  same  size  which 
branch  more  gradually.  The  fact  that  the  internal  cap- 
sule (motor  part)  is  supplied  by  vessels  that  are  often  the 


DIAGNOSIS   OF   THE   NATURE   OF   THE   LESION.     279 

seat  of  miliary  aneurisms  is  of  great  practical  importance, 
since  hemorrhage  in  this  situation  is  a  frequent  cause  of 
hemiplegia. 

The  bursting  of  miliary  aneurisms  is  the  predominant 
cause  of  spontaneous  cerebral  hemorrhage,  but  it  is  cer- 
tainly not  the  sole  cause.  Inflammation  and  degeneration 
(chronic  endarteritis,  obliterating  endarteritis,  atheroma, 
hyaline  degeneration)  may  weaken  the  coats  of  the 
arteries  in  which  they  occur  to  such  a  degree  that  these 
vessels  rupture  without  the  previous  development  of 
miliary  aneurisms. 

Miliary  aneurisms  seem  to  depend  mainly  on  a  primary 
degenerative  process  in  the  arterial  wall,  affecting  chiefly  the 
contractile  and  elastic  elements.  The  muscular  coat  of  the 
vessel  disappears  and  the  intima  and  adventitia  come  in  con- 
tact. The  most  important  known  factors  in  the  production 
of  this  degeneration  are  the  blood  pressure  to  which  the 
arteries  are  subjected,  and  the  degenerative  tendency  that 
exists  in  the  second  half  of  life  and  that  is  associated  with 
atheroma.  Cerebral  hemorrhage  may  occur  without  pre- 
existing changes,  as  atheroma,  in  the  vessel  walls  visible 
to  the  naked  eye,  but  it  is  an  important  fact  that  atheroma 
of  the  larger  vessels  is  present  in  a  large  proportion  of  cases 
of  cerebral  hemorrhage,  even  when  the  hemorrhage  is  due 
to  bursting  of  miliary  aneurisms.  Certain  blood  states, 
notably  purpura,  scurvy,  pernicious  anaemia,  and  leuco- 
cythemia,  may  lead  to  cerebral  hemorrhage,  or  rather  to 
cerebral  hemorrhages,  since  the  extravasations  are  gener- 
ally multiple.  In  many  of  these  cases  it  is  impossible  to 
demonstrate  pathological  changes  in  the  vessels. 

Cerebral  hemorrhage  may  occur  in  any  region  of  the 
brain,  but  is  especially  frequent  in  and  about  the  basal 
ganglia  and  in  the  internal  capsule.  Hemorrhage  into  the 
cortex  is  of  rare  occurrence. 


280        DISEASES    OF   THE    NERVOUS    SYSTEM. 

Hemorrhage  gives  rise  to  symptoms  by  destroying 
nerve  elements,  and  by  compressing  neighboring  struc- 
tures and  irritating  them.  This  irritation  of  the  adjacent 
tissue  elements  is  chiefly  operative  during  and  imme- 
diately after  the  onset,  and,  in  conjunction  with  pressure, 
is  responsible  for  many  indirect  symptoms. 

Hemorrhage  into  the  Spinal  Cord,  from  any  cause  what- 
ever, is  an  exceedingly  rare  occurrence,  and  its  rarity  con- 
trasts strikingly  with  the  frequency  of  cerebral  hemorrhage. 
Primary  hemorrhage  into  the  cord  is  so  uncommon  that 
its  occurrence  has  been  doubted,  and  it  is  certainly  true  that 
the  conditions  which,  in  the  brain,  further  its  production 
seem  to  be  absent  in  the  cord.  The  vessels  to  the  cord 
are  long  and  tortuous  and  the  pressure  within  them  is 
never  high.  Miliary  aneurisms  probably  do  not  occur. 
Secondary  hemorrhage  into  the  cord,  during  inflamma- 
tion of  the  cord,  occasionally  occurs  and  may  readily 
be  mistaken  for  primary  hemorrhage.  Secondary  hemor- 
rhage may  also  occur  from  certain  highly  vascular  tumors 
of  the  cord,  especially  certain  gliomata.  Traumatic 
hemorrhage  is  more  common  than  secondary  hemorrhage 
and  is  especially  apt  to  follow  falls  which  severely  concuss 
the  spine.  Not  infrequently  there  is  hemorrhage  into  the 
central  canal  of  the  cord.  Minute  hemorrhages  into 
the  substance  of  the  cord  often  occur  in  the  course  of 
asphyxial  and  convulsive  diseases  (tetanus,  hydrophobia, 
etc.),  but  they  cause  no  symptoms.  In  all  forms  of 
hemorrhage  into  the  spinal  cord  the  gray  matter  is 
particularly  apt  to  be  involved. 

He77iorrhage  into  the  Mejubranes  of  the  Cora  is  rare. 
The  hemorrhage  may  be  extra-meningeal  or  intra-me- 
ningeal.  The  chief  cause  of  either  form  is  injury.  The 
minute  secondary  extravasations  which  occasionally  occur 
in  the  peripheral  nerves  cause  no  symptoms. 


DIAGNOSIS    OF   THE    NATURE   OF   THE    LESION.     281 

Softening".^The  expression  "  softening  of  the  brain," 
when  correctly  used,  relates  to  an  actual  diminution  of 
consistence  of  the  brain  substance,  due  to  the  disintegra- 
tion of  tissue  elements.  The  term  is,  however,  frequently 
employed  by  the  laity  in  an  entirely  different  sense — that 
is,  to  designa.te  almost  any  variety  of  chronic  mental  fail- 
ure, but  especially  dementia  paralytica  and  simple 
senility. 

Literal  cerebral  softening  may  be  the  result  of  several 
distinct  processes.  Of  these  processes  the  chief  are  in- 
flammation and  arrest  of  blood  supply.  We  shall  con- 
sider here  the  latter  only. 

Arrest  of  blood  supply  depends  on  the  occlusion  of  an 
artery.  This  occlusion  deprives  a  certain  area  of  the 
brain  of  its  nutrition,  because,  in  many  regions  of  the 
brain,  the  terminal  arterioles  do  not  anastomose  suf- 
ficiently to  permit  a  re-establishment  through  the  col- 
lateral circulation  of  the  nutritive  processes  in  the 
dependent  part.  The  tissue  elements,  thus  deprived 
of  nutrition,  lose  their  vitality  and  their  function,  and 
undergo  disintegration — that  is,  softening, — necrotic  soft- 
ening it  is  termed.  The  process  is  also  termed  acute 
softening,  owing  to  the  rapidity  with  which  the  necrosis 
occurs. 

Two  distinct  pathological  processes  may  cause  obstruc- 
tion of  an  artery.  These  are  thrombosis  and  embolism. 
Thrombosis  is  the  formation  of  a  blood  clot  within  a 
vessel  at  the  point  of  obstruction  of  the  vessel.  Obstruc- 
tion from  embolism  depends  on  the  lodgment  of  a  plug — 
usually  derived  from  a  distant  part  of  the  vascular  system 
— in  an  artery  which  is  too  small  to  permit  its  further 
passage.  Thrombosis  is  sometimes  secondary  to  embolism 
from  coagulation  in  the  distal  end  of  an  obstructed  artery, 
and  embolism  is  occasionally  secondary  to  thrombosis, 
from  detachment  and  subsequent  advance  of  a  thrombus, 


282         DISEASES   OF   THE   NERVOUS   SYSTEM. 

but  the  two  processes  are  usually  quite  distinct  and 
separate. 

Thrombosis  of  an  artery  generally  results  from  local 
disease  of  the  arterial  walls,  but  occasionally  it  is  due  to 
morbid  blood  states  in  the  absence  of  any  changes  in  the 
artery.  The  predominant  forms  of  arterial  change  are 
atheroma  and  syphilitic  endarteritis.  Both  atheroma  and 
syphilitic  disease  cause  changes  in  the  arterial  walls, 
which  usually  narrow  the  lumen  and  roughen  the  inner 
surface  of  the  thickened  intima.  The  alteration  of  the 
inner  surface  of  the  vessel  disposes  to  the  formation  upon 
it  of  a  clot.  Any  morbid  blood  state,  or  any  condition 
which  weakens  the  action  of  the  heart,  or  otherwise  leads 
to  the  slowing  of  the  blood  current  through  the  diseased 
vessels  may  facilitate  the  occurrence  of  thrombosis. 

Atheroma  involves  chiefly  the  arteries  at  the  base  of  the 
brain,  especially  the  internal  carotid,  middle  cerebral, 
basilar,  and  vertebral.  Obliteration  of  the  lumen  of  the 
middle  cerebral  or  of  its  branches  causes  softening  in  or 
near  the  central  ganglia  or  internal  capsule.  Occlusion 
of  the  pontine  branches  of  the  basilar  causes  softening  of 
the  pons.  It  is  important  to  note  that  the  atheroma  is 
often  symmetrically  distributed. 

Atheroma  is  of  frequent  occurrence  during  the  second 
half  of  life.  Occasionally  it  occurs  earlier — at  thirty-five 
or  forty  years  of  age.  Its  early  occurrence  is  facilitated 
by  the  existence  of  chronic  diffuse  nephritis,  an  impor- 
tant clinical  fact.  Atheroma  increases  in  frequency  as 
age  advances. 

Syphilitic  endarteritis  leads  to  a  greater  narrowing  of 
the  calibre  of  the  affected  vessel  than  do  other  forms  of 
arterial  disease,  and  sometimes  the  thickened  tissue  for- 
mation may  in  itself  obliterate  the  lumen.  Generally  a 
thrombus  forms  when  the  vessel  is  considerably  narrowed. 


DIAGNOSIS    OF   THE   NATURE    OF   THE   LESION.     283 

The  vessels  involved  in  the  process  are  chiefly  those  of 
the  base,  but  the  small  arteries  are  often  diseased,  and 
may  be  diseased  when  the  changes  in  the  basal  vessels  are 
slight  or  wanting.  The  distribution  of  the  change  may 
be  symmetrical,  but  it  is  usually  irregular. 

Syphilitic  arterial  disease  is  usually  a  result  of  acquired 
syphilis,  and  as  the  arterial  changes  are  commonly  devel- 
oped in  the  course  of  four  or  five  years  after  infection, 
they  are  generally  operative  in  producing  softening  during 
adult  life  and  especially  during  early  adult  life. 

In  Embolism  the  plug  takes  its  source  from  some  point 
between  the  lungs  and  the  artery  which  is  obstructed. .  In 
a  large  majority  of  cases  the  obstructing  embolus  comes 
from  the  heart,  being  derived  either  from  vegetations  on 
the  valves  or  from  a  coagulum  in  the  left  auricle.  The 
embolus  may  come  either  from  the  mitral  or  the  aortic 
valve.  Generally  it  comes  from  the  mitral  valve,  and 
mitral  stenosis  is  the  most  frequent  valvular  cause  of  em- 
bolism. Embolism  occurs  somewhat  less  frequently  in 
the  course  of  chronic  endocarditis  than  in  recent  cases  of 
endocarditis  or  in  the  course  of  fresh  exacerbations  of 
endocardial  inflammation. 

An  embolus  sometimes  takes  its  origin  from  the  aorta, 
when  this  is  the  seat  of  atheromatous  change.  There  is 
some  reason  to  believe  that  minute  emboli  of  septic  ma- 
terial may  pass  through  the  pulmonary  capillaries  and 
find  lodgment  in  the  brain.  Only  capillary  cerebral 
vessels  can  be  obstructed  by  emboli  so  minute  that  they 
do  not  lodge  in  the  lung  capillaries.  If  localized  cerebral 
softening  results  from  the  lodgment  of  septic  material  this 
is  purulent.  There  may  be  multiple  foci  of  septic  soft- 
ening in  the  brain,  and  these  may  coalesce  to  form  ab- 
scesses. Whenever  the  embolus  contains  septic  material 
derived  from  any  part  of  the  vascular  system  (usually  from 


284         DISEASES   OF   THE   NERVOUS   SYSTEM. 

ulcerative  endocarditis),  there  may  be  septic  inflammation 
about  the  obstructed  vessels,  with  clinical  evidences  of 
septic  infection. 

Embolism  occurs  at  all  periods  of  life.  It  is  particu- 
larly frequent  between  adolescence  and  middle  life.  Its 
occurrence  is  usually  associated  with  conditions  which 
are  attended  with  endocarditis — especially  with  acute 
articular  rheumatism,  chorea,  and  scarlet  fever — and 
occasionally  it  results  from  the  endocarditis  which  some- 
times develops  in  the  course  of  acute  specific  diseases. 
Conditions  which  increase  the  coagulability  of  the  blood 
may  favor  the  occurrence  of  embolism  by  the  formation 
of  a  clot  on  diseased  valves  or  in  a  feebly  acting  heart, 
with  subsequent  detachment.  Embolism  from  this  cause 
is  not  very  uncommon  in  the  puerperal  state.  The  same 
blood-state  may  lead  to  the  occurrence  of  thrombosis 
under  similar  circumstances. 

Acute  Softening  of  the  spinal  cord,  from  loss  of  blood 
supply,  is  unknown  as  a  distinct  condition.  The  possi- 
bility of  the  occurrence  of  necrotic  softening  from  vascu- 
lar obstruction  as  the  first  stage  of  inflammation  is 
mentioned  elsewhere. 

Thrombosis  of  Sinuses. — Thrombosis  of  sinuses  of 
the  brain  may  result  (i)  from  any  blood  state  or  con- 
dition of  the  circulation  that  favors  coagulation  (primary 
thrombosis),  or  (2)  from  disease  adjacent  to  the  sinuses 
(secondary  thrombosis). 

Primary  Thrombosis  is  usually  associated  with  pro- 
tracted and  exhausting  disease — for  example,  acute 
specific  fevers,  tuberculosis,  carcinoma,  chronic  sup- 
puration, and  very  frequently,  in  infants,  prolonged 
and  exhausting  diarrhoea.  These  different  causes 
are  operative  in  two  ways — by  weakening  the  action 
of   the   heart,    and    by   increasing   the   coagulability   of 


DIAGNOSIS   OF   THE    NATURE    OF   THE    LESION.     285 

the  blood.  The  superior  longitudinal  sinus  is  by  far 
the  most  frequent  seat  of  sinus  thrombosis,  probably 
because  the  blood  current  through  it  is  exceedingly  slow 
and  feeble.  It  has  been  supposed  that  primary  thrombosis 
occurs  in  cerebral  veins,  as  distinguished  from  sinuses, 
and  that  a  lesion  of  this  nature,  in  the  veins  of  the  con- 
vexity, may  underlie  many  cases  of  infantile  hemiplegia. 
There  is  at  present  little  evidence  that  such  a  process  is 
ever  thus  operative,  but  with  the  present  state  of  our 
knowledge  the  possibility  that  venous  thrombosis  con- 
stitutes the  pathological  basis  of  some  cases  of  infantile 
hemiplegia  cannot  be  denied. 

Secondary  Sinus  Thrornbosis  is  most  often  due  to  caries 
of  cranial  bones,  particularly  of  the  bones  of  the  ear. 
Occasionally  it  results  from  disease  external  to  the  cranium, 
as  erysipelas,  or  carbuncle  of  the  face  or  neck.  Almost 
any  cerebral  sinus  may  be  the  seat  of  secondary  throm- 
bosis, but  the  sinus  affected  is  usually  the  one  nearest  the 
local  disease.  The  local  process  is  generally  ear  disease  ; 
hence  the  superior  petrosal  or  lateral  sinus  is  the  usual 
seat  of  the  thrombosis. 

Local  disease  usually  causes  thrombosis  in  one  of  two 
ways.  The  inflammation  either  passes  directly  to  the  wall 
of  the  sinus,  causing  a  phlebitis,  which  results  in  throm- 
bosis, or  a  clot  passes  by  extension  to  the  sinus  through 
a  vein  leading  from  the  seat  of  the  local  disease  to  the 
sinus.  In  the  former  case  the  wall  of  the  sinus  is  inflamed 
(phlebitic  thrombosis)  ;  in  the  latter  the  wall  of  the  sinus 
is  healthy. 

Inflammation. — Inflammation  of  the  Substance  of  the 
Brain,  as  distinguished  from  inflammation  of  the  mem- 
branes of  the  brain,  is  of  rare  occurrence,  and  when  it 
occurs  is  usually  secondary  in  origin  and  restricted  in  its 
limits.     Acute  cerebritis  may  follow  injury  to  the  head, 


286         DISEASES   OF   THE   NERVOUS   SYSTEM. 

or  bone  disease,  but  constitutes  a  condition  of  little  medi- 
cal interest,  unless  it  is  accompanied  with  meningitis. 
The  cerebritis  of  injury  usually  goes  on  to  the  formation 
of  abscess.  Tumors  are  often  surrounded  by  a  zone  of 
inflammatory  softening,  and  there  is  usually  a  zone  of  in- 
flammation about  foci  of  acute  softening.  Acute  specific 
diseases,  and  septic  conditions  generally,  may  lead  to  the 
formation  of  small  foci  of  encephalitis  containing  many 
micrococci.  An  acute  idiopathic  cerebritis  (polio-enceph- 
alitis) has  been  considered  the  probable  cause  of  many 
cases  of  infantile  hemiplegia.  There  is  as  yet  no  direct 
evidence  that  this  is  the  case,  but  there  is  some  reason  to 
believe  that  such  a  process  may  be  effective  in  a  small  pro- 
portion of  cases  of  sudden  cerebral  palsy  in  children. 

Meningitis. — Itifiammation  of  the  Membranes  of  the 
Brain  is  from  a  medical  standpoint  by  far  the  most  im- 
portant form  of  intracranial  inflammation.  '  Inflammation 
of  the  dura  mater  (pachymeningitis)  is  of  rare  occurrence 
except  after  injury.  A  peculiar  form  of  pachymeningitis 
is  that  known  as  pachymeningitis  interna  hemorrhagica 
or  haematoma  of  the  dura  mater.  The  lesion  in  these 
cases  consists  of  delicate  newly  formed  connective  tissue, 
rich  in  small  blood-vessels,  and  containing  in  its  meshes, 
or  on  its  surface,  the  remains  of  extravasations  of  blood. 

Inflammation  of  the  Pia  Mater ^  or  pia-arachnoid  (lepto- 
meningitis), is  of  very  frequent  occurrence.  The  inflam- 
matory process  may  be  diffuse,  and  affect  chiefly  the 
base  or  the  convexity,  or  it  may  be  localized  within  nar- 
row limits.  Certain  forms  of  meningitis,  dependent  on 
the  grade  or  nature  of  the  inflammatory  process,  may  be 
distinguished.  These  are  simple,  purulent,  tubercular, 
and  syphilitic  meningitis.  It  is  impossible  to  draw  a 
sharp  line  between  all  cases  of  simple  and  purulent  men- 
ingitis.    The    ases  to  be  classed  as  purulent  meningitis  are 


DIAGNOSIS    OF   THE   NATURE   OF   THE   LESION.     28/ 

those  in  which  a  layer  of  purulent  exudate  over  the  mem- 
branes inflamed  is  distinctly  visible  to  the  naked  eye.  All 
cases  of  inflammation  (except  specific  forms)  in  which  the 
amount  of  exudation  or  infiltration  falls  short  of  produ- 
cing a  distinct  purulent  layer  are  to  be  classed  as  simple 
meningitis.  In  many  of  these  cases  of  simple  meningitis 
there  is  merely  a  slight  or  considerable  opacity  and  thick- 
ening of  the  pia  in  certain  parts,  though  the  microscope 
shows  the  presence  of  distinct  and  often  considerable  in- 
filtration of  the  membrane  with  small  spheroidal  cells. 
It  is  difficult  to  say  to  which  class  some  cases  of  menin- 
gitis belong.  The  difference  between  the  two  varieties  of 
inflammatory  change  is  probably  merely  one  of  degree 
and  not  of  kind. 

Simple  or  Non-Purulent  Meningitis  is  considerably  more 
common  than  the  purulent  form.  It  is  sometimes  met  with 
after  insolation  and,  more  frequently,  in  the  course  of 
acute  specific  diseases,  or  without  apparent  cause.  Focal 
lesions  of  the  brain,  such  as  tumor,  abscess,  and  occasion- 
ally softening  or  hemorrhage,  may  excite  a  localized 
simple  meningitis  in  their  vicinity.  Inflammatory  ad- 
hesions between  the  dura  and  pia  mater  frequently  occur 
in  the  neighborhood  of  new  growths. 

Purulent  Meningitis  most  commonly  results  from  ad- 
jacent suppuration.  A  frequent  cause  is  disease  of  the 
middle  ear.  Another  common  cause  of  purulent  menin- 
gitis is  suppuration  in  distant  parts.  Thus  it  is  observed 
in  various  forms  of  pyaemia  and  septicaemia.  It  also  oc- 
curs at  times  in  the  course  of  acute  infectious  diseases. 
The  pathological  changes  in  purulent  meningitis  may 
involve  the  entire  extent  of  the  membranes  or  chiefly 
the  convexity  or  base.  Usually  the  changes  are  ex- 
tensive, and  occasionally  they  extend  to  the  spinal 
meninges.     Purulent  meningitis  is,  of  course,  always  of 


288        DISEASES   OF  THE   NERVOUS   SYSTEM. 

bacterial  origin.  Several  different  forms  of  micrococci 
may  give  rise  to  it. 

Tubercular  Meningitis  is  much  the  most  common 
variety  of  meningitis.  Its  distinctive  character  is  the 
occurrence  of  miliary  tubercles  in  the  pia  in  associa- 
tion with  meningitis  which  generally  possesses  the  appear- 
ances of  simple  meningeal  inflammation  and  is  rarely 
purulent.  The  membranes  at  the  base  are  usually  chiefly 
involved  in  the  inflammatory  exudation,  and  the  distinc- 
tive symptoms  of  the  process  are  those  of  unequal  damage 
to  the  cranial  nerve-roots.  The  products  of  inflammation 
are  especially  abundant  about  the  chiasma,  in  the  inter- 
peduncular space,  and  on  the  inferior  surface  of  the  cere- 
bellum. The  tubercles  themselves  are  usually  seen  as 
minute  translucent  grayish-white  granulations,  which  are 
most  numerous  about  the  smaller  arteries  of  the  pia. 
They  are  apt  to  be  especially  numerous  about  the  vessels 
at  the  commencement  of  the  fissure  of  Sylvius. 

Tubercles  of  the  pia  may  exist  without  the  gross 
appearances  of  meningitis,  and  the  development  of  actual 
meningitis  is  probably  always  preceded  by  the  deposition 
of  miliary  tubercles  in  the  pia.  There  seems  to  be  little 
relation  between  the  number  of  the  tubercles  and  the  extent 
or  degree  of  the  inflammatory  process.  Clinically  it  is 
impossible  to  distinguish  between  cases  of  miliary  tuber- 
culosis of  the  membranes  without  inflammation,  and 
tubercular  meningitis,  since  the  symptoms  of  the  former 
condition  cannot  be  distinctly  separated  from  those  of  the 
latter.  Massive,  or  solitary  tubercle,  however,  not  rarely 
gives  rise  to  the  symptoms  of  tumor  before  the  develop- 
ment of  tubercular  meningitis.  When  such  a  meningitis 
is  grafted  on  a  pre-existing  tuberculous  growth  the 
symptoms  of  the  two  conditions  are  complex  in  char- 
acter. 


DIAGNOSIS   OF  THE   NATURE   OF   THE   LESION,     289 

Tubercular  meningitis  probably  depends  on  the  depo- 
sition of  tubercle  bacilli  in  the  vessels  of  the  pia.  In  a 
very  large  proportion  of  cases  the  tubercular  process  in 
the  meninges  is  secondary  to  a  similar  process  elsewhere. 
In  children  it  is  almost  invariably  associated  with  general 
tuberculosis.  Cases  occur,  however,  in  which  there  are 
no  indications  of  tuberculosis  and  in  which  the  menin- 
gitis appears  to  be  primary.  These  cases  usually  occur  in 
young  adults. 

The  primary  focus  of  tuberculosis  may  be  in  almost 
any  part  of  the  body  that  is  the  seat  of  such  disease.  In 
adults  the  primary  process  is  usually  in  the  lungs.  In 
children  it  is  often  in  the  bronchial,  cervical,  or  mesen- 
teric glands.  Tubercular  meningitis  is  particularly  a 
disease  of  childhood,  but  may  occur  at  any  period  of  life. 

Syphilitic  Meningitis  is  usually  a  chronic  process  of 
limited  extent.  Occasionally  the  inflammatory  products 
involve  the  meninges  of  the  base  or  of  the  convexity  ; 
generally  they  are  limited  chiefly  or  entirely  to  a  small 
region  of  the  base,  especially  of  the  posterior  fossa  of  the 
skull.  The  pia  is  usually  much  thickened  with  the  inflam- 
matory exudation,  and  may  be  glued  to  the  dura.  In  a 
later  stage  of  the  process  the  inflammatory  material  un- 
dergoes organization,  and  thick  layers  of  fibrous  tissue 
may  surround  and  compress  the  nerves  at  the  base. 
When  the  meninges  of  the  medulla  are  the  seat  of  such  a 
chronic  inflammatory  process,  the  openings  of  the  fourth 
ventricle  may  be  obliterated,  with  consequent  internal 
hydrocephalus.  Frequently  syphilitic  meningitis  occurs 
about  a  syphilitic  new  growth  (gumma). 

Infiammation  of  the  Spinal  Cord  is  a  condition  of  fre- 
quent occurrence.  The  morbid  process  may  begin  in  the 
nerve  elements  themselves,  or  in  the  neurogliar  elements, 
and  may  involve  the  gray  substance  or  both  gray  and 


290        DISEASES   OF   THE   NERVOUS   SYSTEM. 

white  substance.  Inflammation  causes  disintegration  of 
the  fibres  and  cells  involved,  and  the  first  gross  alteration 
that  usually  results  is  a  diminution  in  consistence — that 
is,  softening.  In  the  course  of  time  the  inflammatory  pro- 
ducts may  undergo  organization  into  new  connective  tis- 
sue, with  perhaps  an  ultimate  increase  in  the  consistence 
of  the  cord.  When  the  morbid  process  runs  a  chronic 
course,  the  cells  and  fibres  undergo  slower  disintegration, 
and  are  gradually  replaced  by  the  products  of  cell  pro- 
liferation in  the  non-nervous  elements.  If  the  changes 
are  very  chronic,  the  cord  may  be  little  or  not  at  all 
softened  in  consistence.  It  may  be  difficult  in  such  a  case 
to  decide  whether  the  process  in  question  is  really  inflam- 
matory and  not  degenerative  in  character,  and  the  decision 
in  a  doubtful  case  will  depend  much  on  our  conception 
of  inflammation. 

The  mechanism  by  which  myelitis  is  produced  is  ex- 
ceedingly obscure.  In  many  acute  cases  the  inflammation 
is  probably  due  to  the  invasion  of  the  vessels  of  the  cord 
by  micro-organisms.  It  is  certain  that  an  anaemic  necro- 
sis or  softening  of  the  cord  (especially  the  gray  sub- 
stance), from  arrest  of  blood  supply,  may  go  on  to 
inflammation,  and  it  is  not  improbable  that  vascular 
obstruction  by  thrombosis  or  embolism  is  a  more  import- 
ant factor  in  causing  myelitis  than  has  been  supposed. 
The  elements  of  the  cord,  especially  of  the  gray  substance, 
have  very  little  or  no  power  of  repair. 

Inflamrnatioji  of  the  Spinal  Meninges  may  involve  chiefly 
the  dura  (pachymeningitis),  or  the  pia  (leptomeningitis). 
The  process  may  run  an  acute  or  chronic  course.  Acute 
inflammation  rarely  remains  limited  to  the  membrane  in 
which  it  begins  ;  it  extends  to  the  other.  Chronic  inflam- 
mation, on  the  other  hand,  may  remain  limited  to  the 
membrane  (dura  or  pia)  in  which  it  commences.     Hence 


DIAGNOSIS   OF   THE    NATURE   OF   THE   LESION.     29 1 

it  is  only  in  chronic  cases  that  the  symptoms  of  men- 
ingitis can  be  referred  to  one  or  the  other  membrane, 
according  to  their  character,  with  any  degree  of  certainty. 

For  practical  purposes  it  is  convenient  to  divide  menin- 
gitis into  two  forms — external  meningitis,  and  internal 
meningitis. 

External  Meningitis  is  that  form  which  begins  outside 
the  dura  mater.  It  is  probably  always  secondary  to  ad- 
jacent disease,  and  of  such  disease  the  most  frequent 
cause,  by  far,  is  bone  disease — caries.  The  inflammation 
is  usually  purulent  in  character  or  semi-purulent.  Fre- 
quently the  dura  is  covered  by  a  thick  layer  of  soft  or 
hard  cheesy  matter  containing  tubercle  bacilli.  These 
inflammatory  materials,  if  abundant,  may  seriously  com- 
press the  cord,  and  then  the  symptoms  of  compression  are 
combined  with  those  of  inflammation.  The  nerve-roots, 
as  they  pass  through  the  dura,  are  either  irritated  and  in- 
flamed or  compressed  and  atrophied.  The  vertical  extent 
of  the  inflammation  is  usually  limited. 

Internal  Meningitis,  or  inflammation  inside  the  sheath 
of  the  dura,  usually  commences  in  the  pia,  but  may 
extend  to  it  from  the  inner  surface  of  the  dura.  The 
inflammatory  process  may  be  simple  (very  rarely),  puru- 
lent, or  tubercular,  or,  in  chronic  cases,  syphilitic.  The 
causes  of  acute  internal  meningitis  are  often  obscure. 
The  disease  may  follow  exposure  to  cold,  trauma, 
surgical  procedures,  etc.  Sometimes  it  occurs  in  the 
course  of  acute  febrile  diseases  or  septicaemia.  Not 
rarely  it  results  from  extension,  either  from  the  mem- 
branes of  the  brain  or  from  external  meningitis.  The 
symptoms  in  acute  cases  are  :  first,  those  of  irritation  of 
the  nerve-roots,  later  those  of  pressure.  The  inflamma- 
tion is  generally  of  wide  extent  when  it  is  acute.  In  both 
acute  and  chronic  meningitis,  it  must  be  noted,  the  sub- 


292         DISEASES    OF   THE    NERVOUS    SYSTEM. 

Stance  of  the  cord  may  suffer  from  the  inflammation 
(meningo-myelitis),  and  the  symptoms  of  the  two  condi- 
tions are  then  mixed.  Probably  all  cases  of  acute  internal 
meningitis  are  of  bacterial  origin. 

Injlammation  of  Nerves — Neuritis — may  be  acute  or 
chronic,  primary  or  secondary,  interstitial  or  parenchy- 
matous. The  interstitial  form  is  that  in  which  the  con- 
nective tissue  which  separates  the  fibres  is  chiefly  involved. 
In  the  parenchymatous  or  degenerative  variety  the  fibres 
suffer  chiefly  and  primarily.  Secondary  neuritis  may  be 
syphilitic,  tubercular,  cancerous,  or  leprous,  according  to 
the  character  of  the  process  to  which  the  inflammation  is 
secondary.  Syphilitic  and  tubercular  neuritis  affect 
chiefly  the  central  ends  of  nerves,  which  become  involved, 
either  from  the  direct  extension  of  corresponding  inflam- 
matory processes  in  the  meninges,  or  from  similar  inflam- 
miations  in  adjacent  tissues.  Syphilitic  neuritis  frequently 
involves  the  cranial  nerves. 

The  term  neuritis  is  ordinarily  used  to  include  two  dif- 
ferent processes.  First,  it  is  applied  to  those  changes  in 
nerves  which  are  unquestionably  inflammatory  in  origin, 
including  increased  vascularity,  small  spheroidal-celled 
infiltration,  and  the  formation  of  new  connective  tissue, 
with  increase  in  the  size  and  consistence  of  the  nerve. 
Secondly,  the  word  is  employed  to  include  destructive 
changes  in  the  nerve-fibres,  that  extend  down  the  nerve, 
beyond  the  seat  of  the  original  inflammation,  to  the 
periphery.  These  changes  are,  histologically,  essentially 
those  that  occur  in  nerve-fibres  which  have  been  sepa- 
rated partially  or  entirely  from  their  ganglion-cells ; 
they  are  the  changes  of  secondary  or  Wallerian  degener- 
ation (pp.  2  and  6).  In  many  instances  these  degenerative 
alterations  are  not  so  severe  in  degree  as  those  which 
occur,  for  example,  after  nerve-section,  but  they  are  the 


DIAGNOSIS    OF   THE   NATURE   OF   THE    LESION.     293 

same  in  kind.  Slight  evidences  of  inflammation  may 
extend  a  short  distance  down  a  nerve  after  a  traumatism, 
but  the  changes  soon  become  purely  degenerative  in 
character  (p.  2 S3).  Occasionally  a  neuritis  passes  up 
a  nerve  (neuritis  migrans,  ascending  neuritis),  and  the 
changes  are  then  purely  inflammatory  in  nature. 

Generally  one  nerve  trunk  only  is  involved  in  neuritis, 
but  many  nerves  may  suffer  at  the  same  time  in  the  con- 
dition called  multiple  neuritis.  Multiple  neuritis  is  most 
commonly  a  result  of  alcoholism,  but  it  occurs  not  very 
rarely  in  a  variety  of  constitutional  conditions,  of  which 
diphtheria,  lead  poisoning,  and  typhoid  fever  are  the 
principal  (toxic  degenerations).  Injury,  both  slight  and 
severe,  is  a  very  common  cause  of  neuritis.  Extension 
from  adjacent  inflammation  is  also  a  frequent  mode  of 
origin.  When  the  cranial  nerve-roots  or  the  spinal 
nerve-roots  become  the  seat  of  inflammation,  it  is  usually 
by  extension. 

Abscess. — Abscess  of  the  Brain  is  usually  the  result  of 
chronic  suppurative  inflammation  of  the  middle  ear,  of 
traumatism  with  or  without  injury  to  the  skull,  or  of  sup- 
purative processes  at  a  distance, — as,  for  example,  empy- 
sema,  suppurating  cavities  in  the  lungs,  etc.  In  rare 
instances  it  results  from  caries  of  the  nasal  or  orbital 
bones.  Chronic  otitis  is  the  most  common  cause  (about 
42  ^),  and  traumatism  stands  next  in  frequency  (about 
24  f).  Chronic  otitis  is  often  associated  with  caries  of 
the  temporal  bone  or  of  the  mastoid  cells.  The  abscess 
is  usually  in  the  cerebral  or  cerebellar  hemisphere  of  the 
side  of  the  otitis, — nearly  four  times  as  frequently  in  the 
former  as  in  the  latter.  When  the  abscess  follows  dis- 
ease of  the  mastoid  cells  it  is  apt  to  be  in  the  cerebellum. 
Abscess  is  rare  as  a  result  of  pyaemia  cerebral,  and  when 
it  occurs  the  collections  of  pus  are  multiple  and  usually 


294         DISEASES   OF   THE   NERVOUS   SYSTEM. 

small.  In  a  considerable  proportion  of  cases  of  abscess 
(about  one  sixth)  there  has  been  no  discoverable  cause. 

Abscess  may  occur  in  any  region  of  the  brain.  It 
is,  however,  most  frequent  in  the  cerebrum  or  cerebellum, 
and  only  occurs  rarely  in  the  pons,  medulla,  or  basal 
ganglia.  The  collection  of  pus  is  generally  within  the 
substance  of  the  brain,  but  sometimes  it  is  on  the  surface, 
and  in  this  case  the  meninges,  which  are  locally  inflamed 
and  thickened,  form  the  outer  wall  of  the  abscess. 
As  a  rule  there  is  one  abscess  only  (about  four  fifths  of  all 
cases).  When  there  are  two  or  more  abscesses,  they  are 
generally  the  result  of  a  septic  process  at  a  distance. 
When  abscess  is  due  to  ear  disease,  or  follows  traumatism, 
it  is  single  in  about  nine  tenths  of  the  cases.  In  size, 
abscesses  vary  between  that  of  a  hen's  egg  and  a  walnut. 

Symptoms  of  cerebral  abscess  may  be  few  or  absent, 
in  chronic  cases,  for  a  considerable  period  of  time,  some- 
times for  years,  notwithstanding  the  lesion  is  large  and 
in  a  situation  from  which  focal  symptoms  might  be  ex- 
pected. When  acute  symptoms  eventually  commence, 
they  are  often  dependent  on  rupture,  either  into  the  lat- 
eral ventricles,  or  into  the  membranes,  with  subsequent 
ependymitis  in  the  former  case,  with  meningitis  in  the 
latter,  if  the  patient  lives  long  enough.  More  frequently, 
acute  cerebral  symptoms  are  due  to  enlargement  of  the 
abscess  without  rupture.  All  cases  of  cerebral  abscess 
depend  on  micro-organic  infection.  Several  different 
varieties  of  pyogenic  bacteria  appear  competent  to  cause 
cerebral  abscess. 

Abscess  of  the  Spinal  Cord  is  a  condition  of  extremely 
rare  occurrence.  Acute  inflammatory  affections  of  the 
cord  seldom  go  on  to  abscess  formation.  Small  accumu- 
lations of  leucocytes  sometimes  occur  in  the  gray  sub- 
stance of  the  cord  (^.^.,  in  poliomyelitis),  but  these  col- 


DIAGNOSIS   OF   THE    NATURE    OF   THE    LESION.     295 

lections  are  seldom  visible  to  the  naked  eye,  and  can 
never  be  said  to  constitute  abscess.  In  cases  of  purulent 
internal  meningitis,  however,  pus  may  form  in  large 
quantity  in  the  substance  of  the  cord,  and  this  probably 
constitutes  the  only  mode  of  abscess  formation  in  the 
spinal  cord.  The  purulent  meningitis  in  these  instances 
is  always  of  septic  origin.  Thus,  in  one  case,  it  followed 
a  fetid  bronchitis  ;  in  another  it  was  secondary  to  gonor- 
rhoea. Occasionally  abscess  is  secondary  to  traumatism 
(especially  fracture  of  vertebrae). 

The  practical  importance  of  abscess  of  the  spinal  cord 
is  not  great,  as  its  distinction  from  myelitis  is  usually  im- 
possible. Occasionally  acute  irritative  spinal  symptoms, 
associated  with  a  cause  of  septic  suppuration,  may  point 
to  abscess  rather  than  myelitis.  In  many  instances  the 
acute  spinal  symptoms  of  abscess  are  obscured  by  the 
symptoms  of  the  pre-existing  purulent  meningitis. 

Tumor. —  Tumor  of  the  Brain  may  be  of  almost  any 
variety,  but  certain  kinds  are  much  more  common  than 
others.  Syphilitic  and  tubercular  intracranial  growths 
(so-called  diathetic  tumors)  are  more  common  than  other 
varieties.  For  clinical  and  other  reasons  it  is  convenient 
to  speak  of  syphilitic  and  tubercular  growths  as  tumors. 
They  are  not,  however,  tumors  in  the  strict  sense,  and  it 
is  preferable  to  regard  them  as  the  results  of  specific 
forms  of  inflammation.  Next  in  the  order  of  frequency 
come  the  sarcomatous  tumors,  sarcoma  and  glioma. 
Then  comes  carcinoma,  which  is  always  of  the  soft  variety. 
Other  kinds  of  cerebral  tumor  (fibroma,  osteoma,  lipoma, 
neuroma,  echinococcus  and  cysticercus  cysts)  are  rare, 
but  are  occasionally  encountered.  Intracranial  aneurism 
(of  the  larger  vessels),  though  it  does  not  constitute  a  new 
growth,  may  be  classed  clinically  with  tumors  because  of 
its  pressure  symptoms. 


296        DISEASES   OF   THE   NERVOUS    SYSTEM. 

The  cause  of  most  intracranial  tumors  is  obscure. 
Generally  speaking  they  are  twice  as  common  in  males 
as  in  females.  During  the  first  six  months  of  life,  and  in 
old  age,  they  are  rare.  The  majority  of  cases  occur  in 
childhood  and  in  early  adult  life.  Syphilitic  tumors  occur 
chiefly  between  the  twenty-fifth  and  fiftieth  years,  and  in 
consequence  of  acquired  syphilis.  The  time  of  their 
development  after  the  initial  lesion  is  commonly  between 
five  and  ten  years,  but  may  be  considerably  earlier  or 
later.  Three  quarters  of  all  tubercular  tumors  of  the 
brain  occur  before  the  twentieth  year,  usually  in  subjects 
who  have  a  family  history  of  phthisis  or  who  have  signs 
of  pulmonary  tuberculosis. 

Glioma  and  sarcoma  are  most  frequent  during  adult 
life.  Carcinoma  is  exceedingly  rare  before  fifty.  Local 
injury  occasionally  operates  as  an  immediate  excitant  of 
a  new  growth,  and  such  an  influence  has  been  traced  not 
only  in  tumors  which,  like  glioma,  are  supposed  to  be  of 
purely  local  origin,  but  in  the  case  of  the  diathetic  tumors 
(syphilitic  and  tubercular). 

Tumors  may  either  compress  or  infiltrate  the  substance 
of  the  brain  ;  some  do  both.  Growths  that  spring  from 
the  dura  or  from  the  bones  of  the  skull  usually  compress 
but  do  not  invade  the  brain  tissue.  Growths  that  origi- 
nate in  the  brain  substance  or  in  the  pia  may  either  com- 
press or  infiltrate  it.  The  brain  tissue  is  gradually  de- 
stroyed, in  either  case,  before  the  advance  of  the  tumor, 
and  there  is  usually  a  corresponding  loss  of  function, 
though  it  is  important  to  note  that  the  degree  of  functional 
loss  (expressed  as  symptoms)  may  be  much  less  than  our 
knowledge  of  the  functions  of  the  parts  and  the  size  of 
the  tumor  would  lead  us  to  expect.  This  probably  de- 
pends on  the  fact  that  many  of  the  nerve  elements  which 
are  compressed  by,  or  included  in,  the  advancing  tumor 


DIAGNOSIS   OF   THE   NATURE    OF   THE    LESION.     297 

are  not  deprived  of  all  functional  power.  We  have  al- 
ready noted  the  tolerance  of  nerve  elements,  especially 
fibres,  to  gradual  pressure.  The  development  of  a  tumor 
generally  gives  rise  to  irritation,  irritation  which  results 
partly  from  the  pressure  exerted  by  the  growth,  partly 
from  the  vascular  derangement  that  is  associated  with  it. 
This  irritation  may  be  considerable  in  degree,  and,  in  the 
immediate  vicinity  of  the  advancing  tumor,  may  be  in- 
flammatory in  character.  This  is  the  cause  of  the  zone 
of  softening  which  often  surrounds  a  tumor.  The  men- 
inges, and  particularly  the  pia,  are  apt  to  be  inflamed  in 
the  neighborhood  of  the  new  growth,  and  some  meningeal 
inflammation  may  occur  even  at  a  distance  from  a  rapidly 
growing  tumor.  Many  of  the  most  important  and  dis- 
tinctive symptoms  of  tumor  are  referable  to  this  irritation 
incidental  to  their  growth,  and  it  is  an  important  fact  that 
the  degree  and  range  of  these  symptoms  are  often  dispro- 
portioned  to  the  size  of  the  tumor. 

There  remain  to  be  mentioned  certain  individual  forms 
of  tumor  that  possess  some  diagnostic  importance. 

Tubercular  tumors  of  the  brain  are  usually  in  the 
cerebral  substance  but  near  the  surface,  yet  often  un- 
connected with  the  membranes  ;  occasionally  they  spring 
from  the  dura.  Their  most  frequent  seat  is  the  cere- 
bellum, but  they  occur  almost  as  frequently  in  the  cere- 
brum. In  20  fo  of  recorded  cases  they  have  been 
multiple.  They  compress  the  brain  tissue,  and  do  not 
usually  invade  it  to  any  great  extent.  Sometimes  they 
grow  rapidly,  sometimes  slowly  ;  often  they  develop 
rapidly  and  then  become  stationary.  A  tubercular 
growth  may  cause  very  little  irritation. 

Syphilomata  are  usually  superficial  and  connected  with 
the  pia  ;  occasionally  they  spring  from  the  dura.  They 
compress  but  usually  do  not  infiltrate  the  brain.     Their 


298         DISEASES   OF  THE   NERVOUS  SYSTEM. 

chief  seat  is  the  cerebrum,  at  the  base  of  the  brain,  and 
somewhat  less  frequently  they  occur  in  the  central  cor- 
tex, cerebellum,  and  pons.  A  syphiloma  usually  grows 
rather  rapidly  and  causes  considerable  and  often  great 
irritation. 

Gliomata  are  single  nine  times  out  of  ten.  They  de- 
velop in  the  brain  substance,  usually  in  that  of  the  cere- 
brum (one  half  of  the  cases),  often  in  the  cerebellum 
(one  quarter  of  the  cases).  They  invade  the  brain  sub- 
stance without  displacing  it.  They  surround  and  annihi- 
late the  nerve  elements,  and  soon  compass  considerable 
destruction.  The  growth  of  a  glioma  is  usually  slow, 
sometimes  very  slow.  It  does  not  compress  the  brain  as 
do  sarcomata.  All  gliomata  have  a  marked  tendency  to 
undergo  fatty  degeneration  with  central  liquefaction 
{cyst  formation).  The  tumor  is  often  highly  vascular, 
and  is  sometimes  the  seat  of  sudden  hemorrhage,  which 
may  be  indicated  by  an  apoplectic  seizure. 

Sarcomata  may  grow  from  the  brain  substance,  from 
either  membrane,  or  from  bone  (especially  of  the  base). 
Usually  they  do  not  infiltrate  like  gliomata,  but  possess 
distinct  limits,  though  the  softer  varieties  may  have  the  in- 
vasive tendency  of  glioma.  Their  growth  is  usually  slow, 
and  they  are  generally  single.  Carcinoma  may  originate 
from  the  dura  or  the  brain  substance.  It  is  usually  sec- 
ondary to  carcinoma  in  other  parts  of  the  body,  most 
frequently  of  the  orbit  or  the  retina.  It  may  occur  in 
any  part  of  the  brain,  but  is  most  often  observed  in  the 
cerebral  hemisphere.  It  is  usually  single,  and  generally 
both  invades  and  compresses  the  brain  substance 

Tumors  of  the  Spi?ial  Cord. — New  growths  within  the 
spinal  canal  may  originate  external  to  the  dura,  or  inter- 
nal to  the  dura.  The  tumors  that  arise  outside  the  dura 
may  take  their  origin  from  the  membrane  itself,  from  the 


DIAGNOSIS   OF   THE   NATURE   OF   THE   LESION.     299 

extra-dural  tissue  (fat)  or  from  the  adjacent  bones.  Sar- 
comata, carcinomata,  and  enchondromata  occasionally 
spring  from  the  bones  or  intervertebral  substance.  Lipo- 
mata  may  originate  in  the  fat  between  the  dura  and  the 
bone,  but  are  very  rare.  Extra-dural  growths  produce 
symptoms  by  compressing  the  spinal  cord,  and  irritating 
or  compressing  the  nerve-roots  with  which  they  are  in 
contact.  Accumulations  outside  the  dura,  of  inflamma- 
tory nature  from  tubercular  bone  disease  (caries),  give 
rise  to  effects  similar  to  extra-dural  new  growths.  The 
former  are  twice  as  common  as  all  forms  of  tumors  of 
the  cord  and  membranes  combined  ;  all  forms  of  new 
growth  of  the  cord  are  rare.  The  ratio  to  tumors  of  the 
brain  is  one  to  thirteen. 

Of  the  tumors  that  originate  inside  the  dura,  the  ma- 
jority begin  in  the  membrane  rather  than  inside  the  sub- 
stance of  the  cord  itself.  Such  tumors  are  most  often 
syphilitic  ;  less  frequently  they  are  sarcomatous  or  myx- 
omatous. They  compress  the  cord  and  its  nerve-roots, 
and  are  apt  to  damage  the  former  more  seriously  than  do 
extra-dural  tumors,  but  they  do  not  often  invade  the 
substance  of  the  cord,  even  if  they  spring  from  the  pia.  , 

Of  the  new  growths  which  occur  within  the  substance 
of  the  cord  itself,  syphiloma  and  glioma  are  the  most 
common,  or,  more  accurately,  the  least  infrequent.  Sar- 
comata, myxomata,  and  tubercular  tumors  are  rare. 
Syphilomata  usually  spring  from  the  pia,  gliomata  from 
the  peri-ependymal  tissue  immediately  about  the  central 
canal  of  the  cord.  Gliomata  often  have  a  considerable 
vertical  extent,  and,  when  vascular,  are  sometimes  the 
seat  of  hemorrhage,  but  rarely  contain  cysts  as  do  those 
of  the  brain.  Sometimes,  also,  an  extensive  infiltration 
of  the  spinal  cord  with  gliomatous  tissue,  constituting 
gliomatosis,  which  should  not  be  confounded  with  gli- 


300         DISEASES   OF   THE   NERVOUS   SYSTEM. 

oma,  breaks  down  spontaneously  and  leads  to  the  forma- 
tion of  cavities  in  the  cord,  and  which  usually  connect 
with  the  central  canal  of  the  cord, — a  condition  known 
as  syringomyelia. 

Tumors  growing  within  the  substance  of  the  cord  com- 
press and  destroy  the  nerve  elements.  They  are  less 
apt  than  extra-spinal  tumors  to  compress  and  irritate  the 
nerve-roots.  What  has  been  said  of  the  progress  of  the 
different  varieties  of  intracranial  tumors  applies  in  gen- 
eral to  tumors  of  the  cord.  Tumors  of  the  spinal  cord 
are  usually  single,  and  small  or  moderate  in  size.  Sarco- 
mata are  sometimes  multiple  and  very  numerous.  When 
they  invade  the  substance  of  the  cord,  its  tracts  are  fre- 
quently the  seat  of  secondary  degeneration,  ascending 
and  descending.  Malignant  tumors  of  the  cord  are  ten 
times  as  frequent  as  benign  tumors.  Tumors  are  more 
commonly  situated  on  the  posterior  and  lateral  surface 
of  the  cord  than  upon  the  anterior  aspect. 

The  Cauda  Equina  is  occasionally  the  seat  of  a  sarcoma, 
or  fibro-sarcoma.  A  tumor  in  this  region  may  attain  con- 
siderable size  without  producing  pressure  symptoms, 
because  of  the  large  size  of  the  vertebral  canal. 

Tumors  of  the  Peripheral  Nerves  are  occasionally 
observed.  Any  morbid  growth  on  a  nerve  is  called 
a  neuroma,  but  a  distinction  is  made  between  true 
neuromata,  which  consist  of  nervous  tissue,  and  false 
neuromata,  which  contain  no  nervous  elements.  False 
neuromata  are  most  often  hard  fibromata,  occasionally 
sarcomata,  myxomata,  or  gliomata.  Neuromata  gener- 
ally lie  between  the  nerve  bundles,  which  they  push  aside, 
but  do  not  usually  involve.  They  are  usually  single,  but 
may  be  very  numerous.  The  nerves  of  the  extremities 
are  most  often  affected. 


DIAGNOSIS   OF   THE   NATURE    OF   THE   LESION.      3OI 

Degeneration. — The  tissue  elements  of  the  brain, 
and  of  the  spinal  cord,  frequently  undergo  a  gradual 
change  in  structure  known  as  degeneration.  This  change 
consists  of  two  distinct  pathological  processes.  One  of 
these  is  the  slow  wasting  of  the  nerve  elements — the 
gradual  atrophy  of  the  ganglion-cells,  or  nerve  fibres,  or 
both.  The  other  is  an  overgrowth  of  the  interstitial  or 
connective-tissue  (neurogliar)  elements.  It  is  customary 
to  distinguish  two  forms  of  the  degenerative  process — 
that  which  is  confined  to  structures  which  possess  the 
same  or  similar  functions,  and  that  which  is  apparently 
random  in  its  distribution,  and  is  not  limited  to  structures 
having  the  same  function.  The  former  type  of  the  de- 
generative process  is  well  exemplified  by  the  so-called 
"  system  diseases  "  of  the  spinal  cord,  in  which  particular 
(functional)  tracts  of  fibres  are  the  exclusive  seat  of  the 
morbid  process.  Locomotor  ataxia,  in  which  the  poste- 
rior median  columns  of  the  cord  are  degenerated,  and 
primary  lateral  sclerosis,  in  which  the  crossed  pyramidal 
tracts  are  similarly  involved,  are  illustrations  of  system- 
diseases.  Other  examples  are  secondary  degenerations 
— that  is,  degenerations  which  occur  in  the  brain  and  in 
the  spinal  cord,  when  certain  tracts  of  nerve-fibres  have 
been  separated,  from  any  cause,  from  the  ganglion-cells 
that  constitute  their  trophic  centres.  When  the  fibres 
have  been  thus  separated  from  their  nutritive  centres  for 
a  period  of  two,  three,  or  four  weeks,  the  medullary 
sheath  and  the  axis-cylinder  undergo  disintegration,  and 
the  tract  or  tracts  in  which  this  change  occurs  becomes 
gradually  gray  in  color,  somewhat  shrunken,  and  perhaps 
somewhat  harder  than  normal.  In  certain  tracts  these 
secondary  degenerative  changes  progress  in  an  upward  di- 
rection (ascending  degeneration),  in  others  in  a  downward 
direction  (descending  degeneration)  ;  in  general,  the  de- 
pjeneration  progresses  in  the  direction  in  which  the  tracts 


302  DISEASES   OF   THE   NERVOUS   SYSTEM. 

involved  habitually  conduct  nervous  impulses.  Thus  the 
motor  tracts,  the  direct  pyramidal  tract  and  the  crossed 
pyramidal  tract,  undergo  descending  degeneration,  whilst 
the  sensory  tracts,  the  posterior  median  columns,  the 
direct  cerebellar  tracts,  and  the  antero-lateral  ascending 
tracts  (p.  ;^$)  degenerate  in  an  upward  direction.  A 
transverse  lesion  of  the  cord  is  often  the  cause  of  second- 
ary degenerations,  both  of  an  ascending  and  descending 
character.  This  is  well  seen  in  transverse  myelitis  and 
in  certain  tumors  of  the  cord. 

After  hemiplegia  from  any  organic  disease  of  the  brain 
there  is  a  descending  degeneration  of  the  direct  pyrami- 
dal tract  on  the  same  side  and  of  the  crossed  pyramidal 
tract  of  the  opposite  side,  the  degenerative  process  be- 
ginning in  the  motor  path  just  below  the  lesion  in  the 
brain,  whatever  may  be  its  position.  In  the  primary  de-' 
generative  disease  of  the  cortex  known  as  dementia 
paralytica,  there  are  usually  extensive  secondary  degen- 
erations of  the  pyramidal  tracts  of  either  side,  consequent 
on  the  changes  in  the  ganglion-cells  of  the  cortex. 

It  is  highly  probable  that,  in  all  the  system  degenera- 
tions, the  changes  in  the  nerve  elements  are  primary  and 
that  the  interstitial  overgrowth  is  a  secondary  change.  In 
the  second  type  of  degenerative  changes,  on  the  other 
hand,  this  is  not  the  case.  Here  the  alterations  begin,  in 
all  probability,  in  the  interstitial  elements  external  to  the 
nervous  elements,  which  are  involved  secondarily.  A 
good  example  of  this  type  of  degeneration  is  insular 
sclerosis,  in  which  patches  of  degenerative  change  are 
irregularly  scattered  through  the  central  nervous  system. 
Irregular  areas  of  degeneration  in  the  brain  and  spinal 
cord  are  also  observed  in  some  cases  of  the  so-called 
traumatic  neuroses,  and  such  changes  are  probably  more 
frequent  after  traumatism  than  has  been  supposed.    These 


DIAGNOSIS   OF   THE   NATURE  OF   THE   LESION.     3O3 

changes  are  sometimes  associated  with  extensive  hyaline 
and  fatty  degeneration  of  the  cerebro-spinal  arteries. 
Some  instances  of  this  second  type  of  degeneration  are 
probably  intermediate  in  their  pathological  characters 
between  true  degeneration  and  chronic  inflammation. 

The  etiology  of  the  primary  degenerations  of  the  brain 
and  spinal  cord,  affecting  nerve- fibres  or  nerve-cells  or 
both,  is  obscure.  What  is  known  concerning  it  will  be 
alluded  to  elsewhere  in  this  chapter. 

The  structural  changes  which  the  nerve-fibres  of  a 
peripheral  nerve  undergo  after  their  separation  from  the 
cells  to  which  they  belong,  differ  somewhat  in  character 
from  the  changes  of  secondary  degeneration  in  the  cen- 
tral nervous  system.  The  medullary  sheaths  of  the 
nerve-fibres  break  up  into  segments,  and  these  in  turn 
break  up  into  droplets  of  various  size  and  shape.  When 
these  alterations  have  progressed  to  a  certain  point  the 
axis-cylinders  usually  break  up  and  may  be  more  or  less 
completely  destroyed.  The  nerve-fibre  sheaths  (sheaths 
of  Schwann)  and  their  nuclei  do  not  usually  degenerate. 
The  products  which  they  contain  of  the  disintegration  of 
the  medullary  sheaths  may  be  eventually  absorbed.  In  a 
case  of  complete  degeneration  of  a  nerve  from  injury,  the 
complete  segmentation  of  the  myeline  sheaths  and  axis- 
cylinders  is  evidenced  clinically  by  a  loss  of  nerve  irrita- 
bility to  electrical  stimulation.  Such  a  loss  of  irritability 
usually  occurs  at  the  end  of  two  weeks,  but  it  is  not  a 
sudden  loss,  and  is  preceded  by  a  fall  in  irritability  which 
probably  corresponds  to  the  partial  segmentation  of  the 
fibres  and  nutritional  changes  in  the  axis-cylinders.  In 
some  cases  a  slow  process  of  regeneration  occurs  during 
the  second,  third,  and  fourth  month  of  the  injury.  This 
regenerative  process  consists  of  a  development  of  new 
axis-cylinders,  which  in  time  develop  myeline  sheaths,- 
from  the  central  end  of  the  nerve. 


304        DISEASES   OF  THE   NERVOUS   SYSTEM. 

The  causes  of  nerve  degeneration,  which  is  often  a 
partial  process  not  progressing  beyond  a  moderate  degree 
of  structural  change,  are  numerous.  We  may  group  them 
under  three  heads  :  first,  mechanical  injuries,  such  as 
incision,  over-extension,  crushing,  or  compression  ;  sec- 
ondly, disease  of  the  special  nerve  centres  (ganglion-cells 
of  anterior  horns  and  the  motor  cranial  nerve  nuclei) 
with  which  the  peripheral  nerves  are  in  communication,  as 
poliomyelitis  ;  third,  disease  of  the  peripheral  nerves 
themselves,  as  inflammation. 

The  process  which  has  been  here  described  as  degen- 
eration is  regarded  by  some  as  inflam^matory  and  not 
degenerative  in  character,  and  the  condition  has  been 
described  as  one  of  parenchymatous  inflammation.  The 
ordinary  evidences  of  inflammation  are  often  marked  in 
the  neighborhood  of  the  primary  lesion,  but  seldom  extend 
far  below  the  lesion,  where  the  pathological  changes  may 
be  with  propriety  considered  degenerative. 

When  a  motor  nerve  undergoes  degeneration,  changes 
soon  occur  in  the  nutrition  of  the  muscles.  After  a  lapse 
of  ten  days  or  two  weeks  the  muscle  fibres  become  nar- 
rower and  undergo  distinct  changes  in  their  histology. 
If  regeneration  eventually  occurs  in  the  nerve,  the  muscles 
are  gradually  restored  to  their  normal  structure  and  func- 
tion. If  no  regeneration  takes  place,  the  atrophy  of  the 
individual  fibres,  and  of  the  muscles  as  a  whole,  progresses, 
but  the  decrease  in  size  from  muscular  wasting  is  partially 
compensated  by  the  growth  of  connective  tissue  between 
the  muscular  fibres.  This  new  connective  tissue  gradu- 
ally contracts,  and  this  contraction  may  result  in  perma- 
nent shortening  of  the  muscles  involved. 

Having  reviewed  the  general  pathology  and  etiology  of 
the  various  morbid  processes  which  occur  in  the  brain, 


DIAGNOSIS   OF  THE   xVATURE  OF  THE   LESION.     30^ 

spinal  cord,  and  peripheral  nerves,  we  may  pass  to  the 
consideration  of  the  indications  that  serve  to  distinguish 
the  several  lesions.  These  indications  are  of  especial  im- 
portance in  establishing  the  pathological  diagnosis  in 
cases  of  disease  of  the  brain  and  of  the  spinal  cord,  the 
diagnosis  of  the  nature  of  peripheral  affections  being  in 
general  much  simpler.  The  following  considerations  are 
therefore  mainly  applicable  to  disease  of  the  central 
nervous  system. 

The  indications  above  referred  to  as  essential  to  the 
determination  of  the  pathological  diagnosis,  are  the  fol- 
lowing :  first,  the  manner  of  onset  of  the  symptoms^  which 
usually  makes  it  easy  to  distinguish  between  certain 
general  classes  of  morbid  processes  to  be  hereafter  men- 
tioned ;  secondly,  the  causal  indications^  which  comprise  the 
various  causes  of  disease  that  can  be  traced  or  excluded  ; 
thirdly,  the  position  of  the  morbid  process^  taken  in  con- 
junction with  the  special  and  known  liability  of  certain 
parts  of  the  brain  and  cord  to  particular  forms  of  disease. 

I.  The  Onset  of  the  Symptoms. — The  time  oc- 
cupied by  the  onset  of  the  symptoms — that  is,  the  time 
that  intervenes  between  the  first  symptoms  of  the  lesion 
and  their  development  to  a  considerable  degree  of  in- 
tensity— is  an  important  guide  to  the  nature  of  the  lesion. 
If  the  onset  occupies  only  a  few  minutes  or  less,  it  is 
designated  sudden^  and  the  lesion  which  produces  the 
sudden  onset  is  almost  always  a  vascular  lesion  (provided, 
of  course,  that  the  disease  is  organic).  A  vascular  lesion 
in  the  brain  may  be  either  hemorrhage  or  softening  from 
vascular  obstruction  ;  in  the  spinal  cord  such  a  lesion  is 
practically  always  hemorrhage.  If  the  onset,  instead  of 
being  sudden,  occupies  from  an  hour  or  two  to  a  week, 
it  is  described  as  acute.  An  acute  onset  is  usually  indica- 
tive of  an  inflammatory  process,  but  vascular  lesions  are 


3o6        DISEASES   OF  THE   NERVOUS   SYSTEM. 

not  always  sudden  in  their  development,  which  may- 
occupy  a  few  hours  or  days.  When,  therefore,  the  lesion 
develops  in  a  few  hours,  it  may  be  either  vascular  or 
inflammatory  in  nature.  Which  it  is  must  be  determined 
by  the  study  of  other  indications. 

When  the  symptoms  attain  a  considerable  degree  of 
intensity  only  after  the  lapse  of  several  weeks,  the  onset 
is  said  to  be  subacute  ;  and  such  an  onset  usually  charac- 
terizes the  development  of  the  subacute  inflammatory 
processes,  some  forms  of  tumor,  and  in  the  spinal  cord 
also  some  pressure  lesions  not  dependent  on  tumor. 

In  cases  where  the  development  of  the  symptoms 
takes  a  chronic  course — that  is,  occupies  more  than  a 
month — the  morbid  process  is  usually  a  new  growth  or  a 
degeneration. 

Thus  a  knowledge  of  the  mode  of  development  of  the 
symptoms  may  enable  us  at  once  to  roughly  classify  the 
lesion  in  question.  For  instance,  if  the  lesion  is  sud- 
den, it  must  be  vascular  in  character  ;  if  it  is  chronic,  it 
is  probably  a  degeneration  or  a  new  growth.  As  a  rule, 
however,  the  time  of  the  onset  simply  enables  us  to  limit 
the  process  to  one  of  two  lesions.  For  example,  a  case 
which  is  intermediate  between  a  sudden  lesion  and  an 
acute  lesion,  and  occupies  several  hours,  may  be  either 
vascular  or  inflammatory  in  nature.  Beyond  this  point 
the  study  of  the  onset  cannot  take  us  ;  the  decision  de- 
pends on  other  indications. 

II.  The  Causal  Indications. — The  causal  indica- 
tions that  bear  on  the  diagnosis  of  the  nature  of  the 
lesions  of  the  nervous  system  are  numerous  and  import- 
ant. There  is,  however,  a  wide  difference  in  their  rela- 
tive significance,  some  having,  like  age  and  sex,  only  a 
low  value  ;  others,  like  certain  kinds  of  injury  and  cer- 
tain forms  of  infection  (syphilis,  tuberculosis),  possessing 


DIAGNOSIS   OF   THE   NATURE   OF   THE   LESION.     307 

a  value,  under  some  circumstances,  that  is  highly  signifi- 
cant. While  the  causes  which  are  to  be  reviewed  will  of 
course  be  those  that  bear  especially  on  the  organic  dis- 
eases of  the  nervous  system,  it  will  be  well  to  touch  on 
some  of  the  relations  of  these  causes  to  the  functional 
forms  of  nervous  disease. 

The  relations  of  each  etiological  condition  will  be 
given  to  each  class  of  lesion  (hemorrhage,  degeneration, 
tumor,  etc.)  in  so  far  as  is  practicable  or  desirable,  and 
when  profitable  the  more  important  relations  between 
these  conditions  and  particular  clinical  types  of  disease 
will  be  briefly  stated. 

It  is  convenient  to  group  the  etiological  factors  to  be 
reviewed,  as  follows  :  age,  sex,  habits,  infection,  toxic 
influences,  trauma,  state  of  general  health,  psychic  influ- 
ence, heredity,  influence  of  treatment. 

Age. — A  knowledge  of  the  age  at  which  the  various 
morbid  processes  occur  is  sometimes  of  considerable 
value  in  determining  the  nature  of  a  lesion.  With  most 
processes,  however,  the  occurrence  extends  over  so  wide 
a  period,  with  so  nearly  equal  incidence  in  several  dec- 
ades,  as  to  deprive  the  age  factor  of  decided  significance. 
The  vascular  lesions  of  the  nervous  system  are  met 
almost  exclusively  in  the  brain.  Regarded  as  a  group, 
these  vascular  lesions  (including  hemorrhage,  embolism, 
thrombosis)  occur  at  all  times  of  life,  but  the  various 
members  of  the  group  are  especially  frequent  at  particu- 
lar periods.  Thus,  embolism  is  rare  after  fifty  and  be- 
fore puberty  ;  syphilitic  thrombosis  occurs  chiefly  in  the 
third,  fourth,  and  fifth  decades,  and  both  hemorrhage 
and  thrombosis  from  atheroma  are  diseases  practically 
limited  to  the  second  half  of  life.  The  vascular  lesions 
which  depend,  like  extra-dural  hemorrhage  and  spinal 
meningeal  hemorrhage,  on  injury,  occur  especially  during 


308        DISEASES   OF   THE   NERVOUS   SYSTEM. 

early  adult  life  (twenty  to  forty).  The  inflammatory  pro- 
cesses, like  the  vascular  lesions,  occur  at  every  period  of 
life,  but  are  on  the  whole  most  common  in  early  adult 
life  and  infancy.  This  is  especially  true  of  the  acute 
inflammations.  Thus,  acute  cerebral  meningitis  and 
cerebro-spinal  meningitis  are  relatively  most  common 
before  the  twentieth  year,  and  although  purulent  menin- 
gitis is  a  disease  of  adult  life  especially,  this  is  due 
mainly  to  the  usual  traumatic  origin'  of  the  disease. 
Acute  poliomyelitis,  by  far  the  most  common  inflamma- 
tory affection  of  the  substance  of  the  central  nervous 
system,  is  essentially  a  disease  of  infancy  and  childhood. 
An  acute  spinal  lesion  occurring  in  infancy  or  child- 
hood is  almost  certainly  poliomyelitis.  Acute  myelitis 
occurs  particularly  between  ten  and  forty.  The  various 
forms  of  inflammation  of  the  peripheral  nerves  (multiple 
neuritis,  neuritis),  acute  and  sub-acute,  are  particularly 
common  in  early  adult  life.  More  than  one  half  the 
cases  of  cerebral  abscess  occur  between  ten  and  thirty 
(partly  due  to  the  influence  of  trauma).  The  more 
chronic  inflammatory  processes,  both  of  the  central  nerv- 
ous system  and  of  the  peripheral  nerves,  probably  occur, 
as  a  rule,  later  in  life  than  the  acute  lesions  (for  example, 
chronic  pachymeningitis,  chronic  myelitis,  chronic  sciatic 
neuritis) 

The  best  example  of  the  influence  of  age  is  found  in 
the  case  of  the  degenerative  affections,  of  which  proba- 
bly more  than  two  thirds  of  the  cases  commence  between 
the  thirtieth  and  fiftieth  years.  This  group  includes  loco- 
motor ataxia,  primary  spastic  paraplegia,  ataxic  paraple- 
gia, general  paralysis,  progressive  muscular  atrophy,  etc. 
There  are,  however,  some  exceptions  to  the  rule  of  com- 
mencement between  the  ages  of  thirty  and  fifty.  Bulbar 
paralysis  often  begins  after  fifty,  insular  sclerosis  most 
often  begins  between    twenty  and  thirty-five,  and  Fried- 


DIAGNOSIS   OF   THE   NATURE   OF   THE   LESION.     305 

reich's  ataxia  most  often  between  seven  and  twenty.  But 
these  cases  form  a  very  small  proportion  of  all  the  cases 
of  degenerative  disease. 

As  a  class  the  new  growths  show  no  striking  features  in 
relation  to  age.  They  are  rare  in  infancy  and  after  sixty. 
The  most  frequent  forms  (tubercle,  glioma,  syphiloma) 
belong  particularly  to  the  first  half  of  life,  the  tubercular 
and  gliomatous  forms  being  most  often  observed  between, 
five  and  thirty,  and  the  syphilomata  between  twenty  and 
forty.     Carcinomata  belong  to  the  second  half  of  life. 

The  group  of  so-called  functional  nervous  diseases  be- 
longs largely  to  the  adolescent  period  and  early  adult  life 
(fifteen  to  thirty-five).  This  is  conspicuously  the  case 
with  the  most  common  forms,  chorea,  epilepsy,  hysteria, 
neuralgia,  and  migraine.  Paralysis  agitans  is,  however,  an 
exception,  in  that  its  period  of  greatest  frequency  is  be- 
tween forty  and  sixty.  Wry-neck  and  neuralgia  also 
occur  very  frequently  between  thirty-five  and  fifty,  but 
these  cases  do  not  in  any  way  invalidate  the  truth  of  the 
general  statement  made  above. 

Sex. — Looking  at  nervous  diseases,  in  so  far  as  we  can, 
as  a  class,  it  is  difiicult  to  say  in  which  sex  they  prepon- 
derate. Certain  it  is,  however,  that  to  the  male  sex  be- 
longs considerably  more  than  half  of  all  the  cases  of 
organic  disease.  This  special  liability  on  the  part  of  the 
male  appears  to  depend  mainly  on  the  effects  of  injury, 
alcohol,  and  syphilis,  to  all  of  which  he  is  more  exposed 
than  the  female.  The  functional  forms  of  nervous  disease 
are  more  frequent,  as  a  class,  in  females,  owing  mainly 
to  the  preponderance  of  two  common  diseases,  hysteria 
and  chorea.  In  paralysis  agitans,  migraine,  and  tetanus, 
the  greater  number  of  cases  occur  in  males — in  the  case 
of  tetanus  the  large  preponderance  depending,  no  doubt, 
on  the  greater  exposure  of  the  male  to  injuries  favoring 
the  necessary  infection. 


310         DISEASES   OF   THE   NERVOUS   SYSTEM. 

The  greater  prevalence  of  organic  disease  in  males  is 
particularly  noticeable  in  the  group  of  degenerative  affec- 
tions. 

In  the  case  of  locomotor  ataxia  the  unequal  incidence 
in  the  sexes  is  very  striking, — being  probably  at  least  ten 
to  one  in  favor  of  males.  An  even  greater  inequality  is 
noticeable  in  an  allied  degenerative  disease — dementia 
paralytica.  A  less  striking  inequality  obtains  in  ataxic 
paraplegia  and  progressive  muscular  atrophy.  Among 
the  inflammatory  processes  there  is  a  marked  preponder- 
ance in  males  of  those  conditions  that  depend  to  a  con- 
siderable extent,  or  mainly,  on  injury, — as  acute  myelitis, 
meningitis  of  the  convexity,  and  abscess  of  the  brain 
(two  to  one),  on  alcohol  (multiple  neuritis,  pachymenin- 
gitis), or  on  syphilis  (as  syphilitic  endarteritis,  chronic 
meningitis,  etc.).  With  the  possible  exception  of  embolic 
softening,  the  vascular  lesions  preponderate  slightly,  and 
in  the  case  of  cerebral  hemorrhage,  largely,  in  males. 

The  indications  of  the  nature  of  the  lesion  which  are 
derived  from  the  consideration  of  age  and  sex,  are,  of 
course,  to  be  regarded  as  quite  subsidiary  to  the  indica- 
tions obtained  from  other  causal  factors.  Some  of  the 
factors  which  have  been  mentioned  may,  however,  be 
allowed  weight  when  the  more  important  indications,  in 
a  given  case,  appear  evenly  balanced,  and  occasionally 
the  facts  noted  will  prove  of  real  service  in  diagnosis. 

Habits. — A  variety  of  influences  in  the  production  of 
nervous  disease,  which  might  properly  be  classed  as  habits, 
could  be  enumerated,  but  of  these  there  is  only  a  small 
number  that  deserve  special  attention.  The  excessive  use 
of  alcohol  and  tobacco,  and  sexual  excess,  including  mas- 
turbation, belong  to  this  class.  Of  these  influences,  al- 
coholic excess  is  by  far  the  most  important  as  regards  the 
causation  of  organic  disease. 


DIAGNOSIS   OF   THE   NATURE   OF  THE   LESION.     311 

Excessive  Use  of  Alcohol. — A  history  of  the  exces- 
sive use  of  alcoholic  drink  serves  to  clear  up  the  nature  of 
a  variety  of  affections  of  the  nervous  system.  It  is  im- 
portant, however,  to  distinguish  between  the  acute  dis- 
turbances from  alcoholic  intoxication  and  the  different 
morbid  states  of  the  nervous  system  that  develop  grad- 
ually as  a  consequence  of  habitual  excess.  The  most  im- 
portant form  of  acute  disturbance  from  alcohol  is  de- 
lirium tremens  (p.  5  9  6)  or  acute  alcoholic  delirium  ;  other 
forms  of  pathological  interest  are  the  various  manifesta- 
tions of  alcoholic  insanity — maniacal,  melancholic,  etc. 
These  acute  alcoholic  insanities  are  commonly  associated 
with  hereditary  predispositions  to  mental  derangement. 
The  common  variety  of  acute  alcoholic  intoxication, 
known  as  "  intoxication  "  par  excellence^  does  not  con- 
cern us. 

A  feature  of  practical  importance  in  the  causation  of 
various  forms  of  nervous  disturbances  that  are  slowly 
induced  by  habitual  excess  is  that  they  may  occur  in 
persons  whose  excess  has  always  fallen  short  of  actual 
intoxication.  It  may  thus  become  difficult,  in  a  given 
case,  to  say  what  constitutes  excess.  The  daily  quantity 
of  alcohol  that  is  borne  without  detriment  varies 
much  with  different  individuals,  and  with  the  same  in- 
dividual at  different  times  and  in  different  conditions  of 
health.  Sedentary  occupations  are  particularly  unfavor- 
able to  the  perfect  assimilation  of  considerable  quantities 
of  alcohol.  Probably  most  adult  males  can  safely  dispose 
of  the  equivalent  of  two  ounces  of  absolute  alcohol  in  a 
day — many  of  much  more,  and  some  undoubtedly  develop 
disease  from  the  habitual  use  of  smaller  quantities.  It 
results  chiefly  from  the  stronger  forms  of  alcohol,  espe- 
cially from  spirits,  but  the  prolonged  and  excessive  use 
of  beer  seems  particularly  apt  to  lead  to  multiple  neuritis. 


312        DISEASES    OF   THE   NERVOUS    SYSTEM. 

The  organic  diseases  that  might  be  accounted  for  by  a 
history  of  alcoholic  excess  are  chiefly  subacute  or  chronic 
in  course,  and  inflammatory  in  character.  To  these  in- 
flammatory lesions  the  peripheral  nerves  appear  especially 
prone.  Thus,  by  far  the  most  frequent  organic  affection 
from  alcohol  is  multiple  alcoholic  neuritis.  Neuralgic 
pains  in  the  limbs,  without  atrophy  or  weakness,  are  com- 
mon as  a  result  of  alcoholic  excess.  They  depend  some- 
times on  slight  acute  neuritis  (sensory  form),  sometimes 
on  functional  (nutritional)  changes.  Subacute  and 
chronic  myelitis,  with  or  without  neuritis,  are  occasional 
results. 

Of  the  cerebral  affections  that  may  depend  on  alcohol, 
slight  chronic  meningitis  (with  slight  optic  neuritis,  head- 
ache, and  mental  failure)  is  the  most  common,  but  habit- 
ual alcoholic  excess  favors  atheroma  of  the  walls  of  the 
cerebral  arteries  and  is  then  a  factor  in  producing  cere- 
bral hemorrhage.  Two  closely  allied  degenerative  affec- 
tions of  the  central  nervous  system — general  paralysis 
and  locomotor  ataxia — occur  frequently  in  alcoholics, 
but  it  is  doubtful  whether  alcohol  is  ever  the  sole  cause 
of  either  disease.  Some  cases  of  chronic  alcoholic  men- 
ingitis closely  resemble  general  paralysis  (pseudo  general 
paralysis).'  Atrophy  of  the  optic  nerve  probably  never  re- 
sults from  alcoholic  excess  alone.  Epilepsy  is  apparently 
an  occasional  consequence.  Hemianaesthesia  (of  uncer- 
tain nature)  is  said  to  depend  at  times  on  alcoholism.  By 
far  the  most  common  nervous  affection  that  results  from 
the  habitual  abuse   of  alcohol  is  a  fine  irregular  tremor 

'  A  special  form  of  psychosis  (Korssakow's  disease)  not  infre- 
quently accompanies  alcoholic  polyneuritis.  The  disease  is  marked 
by  disturbance  of  attention,  defective  memory,  and  pronounced  fabri- 
cations. Its  pathological  anatomy  consists  in  marked  atrophy  of 
the  cerebral  cortex. 


OIAGNOSIS   OF   THE   NATURE   OF   THE    LESION.     313 

involving  the  lips,  tongue,  and  hands,  and  often  the 
legs — alcoholic  tremor.  Such  habitual  abuse  also  strongly 
favors  the  development  of  occupation  neuroses  and  the 
muscular  atrophies  from  over-use. 

The  Excessive  Use  of  Tobacco  (by  smoking  or  chewing), 
appears  to  give  rise  to  but  few  organic  diseases  of  the 
nervous  system.  The  principal  condition  consequent  upon 
such  excess  is  a  peculiar  form  of  amblyopia  characterized 
by  the  existence  of  central  scotomata,  especially  for  the 
colors  green  and  red.  A  variety  of  functional  disturb- 
ances may  be  accounted  for  by  the  habitual  excessive 
use  of  tobacco — headache,  tremulousness,  insomnia,  ir- 
ritability, palpitation,  tachycardia,  blepharospasm  and. 
various  digestive  disorders. 

Sexual  Excess  is  an  exceedingly  rare  cause  of  organic 
disease  of  the  nervous  system,  but  a  common  cause  of 
functional  derangements.  Repeated  sexual  acts  have 
been  the  cause,  in  males,  of  hemorrhage  into  the  lumbar 
enlargement  of  the  cord,  followed  in  some  cases  by  mye- 
litis. In  some  cases  these  conditions  have  resulted  in 
males  from  coition  (not  necessarily  repeated)  in  the  erect 
position.  A  much  less  unusual  effect  of  repeated  sexual 
intercourse  is  transient  weakness,  slight  or  consider- 
able, of  the  lower  extremities.  This  depends  probably 
on  temporary  nutritional  derangement  of  the  anterior 
cornual  cells  of  the  lumbar  cord ;  perhaps  in  some 
instances  on  minute  extravasations. 

The  sexual  act  several  times  repeated  has  in  rare  in- 
stances been  the  exciting  cause  of  hemiplegic  attacks  in 
persons  with  atheromatous  cerebral  arteries.  Similarly, 
persons  with  syphilitic  arterial  disease  have  been  known 
to  become  hemiplegic  after  one  or  more  sexual  acts.^ 

^  In  one  case  of  this  kind  the  autopsy  showed  the  presence  of  acute 
softening.    The  patient  was  a  woman,  and  the  paralysis  came  within 


314        DISEASES   OF   THE   NERVOUS   SYSTEM. 

The  functional  nervous  derangements  which  are  the 
remote  consequence  of  sexual  excess  are  numerous  and 
varied.  They  include  the  protean  manifestations  of 
neurasthenia  and  hysteria.  Especially  common,  how- 
ever, are  irritability,  slight  mental  failure,  headache  and 
other  cephalic  sensations  than  pain,  dilated  pupils, 
amblyopia,  palpitation,  various  vasomotor  symptoms 
(flushing,  etc.),  fibrillary  twitchings,  mental  depression, 
undue  fatigue,  oxaluria,  phosphaturia,  and  digestive  dis- 
orders. These  symptoms  are  of  far  more  frequent 
occurrence  in  men  than  in  women.  In  those  who  are 
subject  to  epilepsy,  sexual  indulgence  occasionally  deter- 
mines the  occurrence  of  paroxysms.  Wry-neck  sometimes 
appears  to  be  due  solely  to  sexual  excess. 

Masturbaton. — It  is  exceedingly  doubtful  whether 
masturbation  is  ever  a  cause  of  organic  nervous  disease, 
though  it  may  very  remotely  influence  the  course  and 
development  of  such  disease.  The  functional  derange- 
ments consequent  on  this  habit  are,  however,  numerous, 
and  of  frequent  occurrence.  The  derangements  resemble 
in  character  the  neurasthenic  symptoms  mentioned 
as  dependent  on  sexual  excess,  with  the  general 
difference  that  they  frequently  attain  a  greater 
degree  of  severity.^     A  mental  symptom  which  is  some- 

a  few  minutes  after  the  sexual  act.  It  is  probable  that  the  circulatory 
changes  in  the  brain  which  follow  and  accompany  violent  sexual  ex- 
citement may  determine  the  occurrence  of  vascular  lesions  in  such 
cases  as  that  mentioned. 

'  Sexual  excitement  is  probably  always  followed  by  an  increase  of 
indican  in  the  urine.  Normally  this  substance  is  present  in  the  urine 
in  very  small  quantities  or  is  entirely  absent.  The  presence  of  more 
than  .020  gm.  of  indican  in  the  twenty-four  hours'  urine  is  to  be 
regarded  as  pathological.  Although  other  causes  than  sexual 
excitement  may  cause  an  increase  of  indican  in  the  urine,  such 
increase  is  sometimes  a  valuable  aid  in  the  detection  of  the  habit  of 
masturbation. 


DIAGNOSIS   OF   THE  NATURE   OF   THE   LESION.     315 

what  characteristic  of  masturbational  excess,  though  it 
sometimes  occurs  in  cases  of  ordinary  sexual  excess,  is  a 
pecuHar  disposition  to  ramble  from  one  topic  of  con- 
versation to  another  in  a  superficial  or  incoherent  manner. 
Sometimes,  again,  there  is  a  morbid  tendency  to  drowsi- 
ness during  the  day,  and,  in  rare  cases,  young  subjects 
have  been  in  stupor  for  many  days  as  a  consequence  of 
repeated  acts  of  masturbation. 

The  evil  results  of  masturbation  are  more  equally  distri- 
buted between  the  sexes  than  are  those  of  sexual  excess. 
Though  most  common  among  individuals  between  the  age 
of  puberty  and  the  twentieth  year,  masturbation  is  often 
practised  by  much  younger  subjects.  The  habit  is  not 
rarely  begun  in  young  children  by  the  teaching  of  lascivious 
nursery-maids.  Not  infrequently  it  originates  in  young 
children  from  genital  irritation  due  to  the  passage  of  the 
irritating  urine  that  commonly  results  from  digestive 
derangements. 

The  proportion  of  persons  (of  each  sex)  who  practise 
masturbation  at  some  period  of  life  is  probably  very  large. 
In  the  majority  of  instances  the  habit  is  not  continued 
sufficiently  long  or  with  sufficient  perseverance  to  give  rise 
to  serious  functional  disturbances. 

Infection. — The  introduction  of  pathogenic  micro- 
organisms into  the  body  is  the  essential  condition  of 
infection.  After  these  have  obtained  mechanical  lodg- 
ment in  some  part,  local  and  general  conditions,  but  im- 
perfectly understood,  determine  their  pathogenic  influence. 
An  extension  (direct  or  through  the  blood  or  lymph 
channels)  of  infection  from  the  parts  first  involved  may 
lead  to  the  implication  of  the  nervous  system,  and  such 
infection  constitutes,  perhaps,  the  most  important  class  of 
influences  in  the  production  of  organic  disease  of  the 
nervous  system.     Two    specific  forms    of   infection,  the 


3l6         DISEASES   OF   THE   NERVOUS   SYSTEM. 

tubercular  and  the  syphilitic,  concern  us  especially,  since 
they  play  a  most  conspicuous  part  in  the  causation  of 
organic  disease.  The  infection  which  results  in  suppura- 
tive processes  in  the  nervous  system  (abscess,  suppurative 
meningitis,  etc.)  is  considered,  for  clinical  reasons,  under 
other  headings. 

Tubercular  Infection. — The  organic  conditions  of  the 
nervous  system  which  result  from  the  invasion  of  tubercle 
bacilli  from  primary  foci  of  infection  are  chiefly  inflam- 
matory in  character.  By  far  the  most  frequent  of  these 
inflammatory  conditions  is  tubercular  meningitis.  In 
infancy  and  childhood  this  is  much  the  most  common 
form  of  cerebral  disease.  In  connection  with  tubercular 
meningitis,  or  occurring  quite  independently,  there  may 
be  an  agglomeration  of  tubercles  in  the  substance  of  the 
brain,  constituting  one  or  more  massive  or  conglomerate 
tubercles  (so-called  "  solitary  "  tubercle  or  "  tubercular 
tumor  ").  Much  less  frequently  the  spinal  cord  is  the  seat 
of  solitary  tubercle,  which  produces  the  symptoms  of 
tumor.  The  peripheral  nerves  are  involved  in  a  neuritic 
affection  in  some  cases  of  advanced  tubercular  cachexia, 
and  this  affection  has  been  regarded  as  a  multiple  neuritis 
of  tubercular  origin.  The  correctness  of  this  view  is 
rendered  somewhat  questionable  by  the  fact  that  the  class 
of  patients  in  whom  the  affection  occurs  (advanced  con- 
sumptives), is  a  class  in  whom  alcoholic  stimulants  are 
extensively  employed  in  treatment.  Conditions  are  pres- 
ent, therefore,  which  favor  the  occurrence  of  alcoholic 
neuritis,  and  it  is  possible  that  many  of  the  cases  which 
pass  for  tubercular  multiple  neuritis  are,  in  reality,  in- 
stances of  alcoholic  neuritis. 

The  forms  of  tubercular  disease  of  the  nervous  system 
above  enumerated,  depend,  with  the  exception  of  the 
neuritis  above  mentioned,  on   the  presence  of   tubercle 


DIAGNOSIS   OF   THE   NATURE   OF   THE    LESION.     317 

bacilli  in  the  tissues  of  the  parts  affected.  Such  local 
deposition  is  not  usually  the  case  with  one  of  the  most 
frequent  consequences  of  tubercular  disease,  the  so-called 
compression  myelitis.  Here,  the  lesion  is  a  tuberculosis 
of  the  vertebrae,  which  leads  to  the  accumulation  of 
tubercular  material  outside  a  thickened  dura,  and  conse- 
quent compression  of  the  cord.  The  compression  of  the 
cord  causes  a  diminution  in  its  size,  and  sometimes  an 
actual  myelitis.  But  the  myelitis  which  results  from 
compression  is  only  rarely  tubercular  in  character, 
and  when  this  is  the  case  the  inflammation  is  derived 
from  a  direct  extension  from  the  outer  surface  of  the 
dura  to  the  pia,  and  from  the  pia  to  the  substance  of 
the  cord.  In  these  cases  there  is  probably  always  the 
formation  of  tubercles  in  the  cord  before  the  actual 
myelitis  develops. 

The  tubercular  affections  of  the  nervous  system  may 
be  secondary  to  tubercular  processes  in  a  variety  of  sit- 
uations. In  adults,  the  primary  lesion  is  usually 
pulmonary  tuberculosis  ;  in  children,  there  is  commonly 
general  miliary  tuberculosis,  and  the  primary  focus 
may  be  tubercular  bronchial  nodes,  interstitial  tuberculo- 
sis, tubercular  bone  disease  (especially  knee  and  hip),  or 
tubercular  teno-synovitis.  In  adults,  the  genito-urinary 
system  is  sometimes  the  seat  of  the  lesion.  In  the  male, 
the  testicle,  prostate,  and  seminal  vesicles  may  be  affected  ; 
in  the  female,  the  uterus  and  Fallopian  tubes.  Thus  the 
infection  which  terminates  in  tubercular  disease  of  the 
nervous  system,  may  make  its  entrance  by  way  of  the 
respiratory  tract,  the  digestive  tract,  the  genito-urinary 
tract,  or  through  slight  injury  to  the  skin  at  any  point. 
In  some  cases  the  evidences  of  local  tuberculosis  are  dis- 
tinct (as  in  chronic  pulmonary  tuberculosis,  or  hip  disease), 
and  give  most  important  indications  for  diagnosis,  but  it 


3l8         DISEASES   OF   THE   NERVOUS   SYSTEM. 

is  essential  to  note  that  in  many  cases  the  original  lesion 
is  so  obscure  in  its  symptomatology  as  to  afford  no  indi- 
cations whatever  of  the  character  of  the  lesion  within  the 
nervous  system.  Hence  it  is  that  the  nervous  lesions 
often  have  the  aspect  of  primary  affections.  While, 
therefore,  the  presence  of  tuberculosis  in  some  part  of 
the  body  other  than  the  nervous  system  may  be  of  the 
highest  aid  in  determining  the  nature  of  the  nervous 
lesion,  the  absence  of  indications  of  such  disease  should 
carry  very  little  weight  if  the  symptoms  themselves  sug- 
gest a  tubercular  process. 

Syphilitic  Infection. — No  form  of  infection  gives  rise 
with  such  frequency  to  organic  disease  of  the  nervous 
system  as  syphilis.  Of  the  organic  conditions  that  arise 
from  syphilitic  infection,  some,  like  gummatous  growths, 
are  processes  which  are  distinctive  of  syphilis  and  never 
occur  as  the  result  of  any  other  cause  than  syphilis. 
Others,  like  certain  degenerative  processes  of  the  brain 
and  cord  (locomotor  ataxia,  progressive  muscular  atrophy, 
etc.),  though  commonly  dependent  on  syphilis,  may  arise 
from  other  causes,  and  possess  no  pathological  features 
that  are  distinctive  of  syphilis.  It  is  important,  in  think- 
ing of  the  consequences  of  syphilitic  infection,  to  bear  in 
mind  these  differences  in  the  relations  of  its  effects. 

Both  the  brain  and  spinal  cord  are  very  frequently  the 
seat  of  organic  disease  which  is  the  consequence  of 
syphilitic  infection.  Of  the  specific  syphilitic  processes 
(gumma,  endarteritis),  the  brain  is  a  much  more  common 
seat  than  the  cord. 

The  chief  vascular  lesion  of  the  nervous  system,  of 
syphilitic  origin,  is  acute  softening  of  the  brain  from  the 
thrombosis  of  cerebral  vessels  that  results  from  syphilitic 
endarteritis.  This  is  a  very  important  and  frequent 
clinical  condition  (p.  282).    Whether  syphilitic  endarter- 


DIAGNOSIS   OF   THE   NATURE   OF   THE   LESION.     319 

itis  of  the  vessels  of  the  cord  is  a  cause  of  focal  softening 
and  inflammation  of  the  cord  cannot  be  positively  stated, 
but  there  is  some  reason  to  believe  that  it  may  not  rarely 
give  rise  to  these  conditions.  A  much  more  rare  effect 
of  syphilitic  vascular  disease  is  intracranial  aneurism. 

An  important  class  of  syphilitic  lesions  is  inflamma- 
tory in  character.  The  clinical  conditions  which  belong 
to  this  group  are  characterized  by  their  subacute  or  sub- 
chronic  course.  This  group  includes  pachymeningitis, 
cerebral  and  spinal,  and  leptomeningitis.  Cerebral  syphi- 
litic meningitis  is  usually  local.  In  the  cord,  inflamma- 
tion of  the  pia  is  seldom  local,  and  is  usually  associated 
with  pachymeningitis.  Inflammation  of  the  substance 
of  the  brain  and  cord,  possessing  the  pathological 
characters  of  a  syphilitic  process,  probably  does  not 
occur.  Whether  acute  myelitis  is  ever  due  to  syphilis 
it  is  as  yet  impossible  to  say.  Subacute  disseminated 
myelitis  probably  depends  in  some  cases  on  syphilis,  but 
its  precise  relations  to  the  disease  are  not  fully  under- 
stood. Whether  syphilitic  infection  ever  leads  to  multiple 
neuritis  must  be  regarded  as  uncertain.  If  it  does  ever 
cause  multiple  neuritis,  it  must  be  in  very  rare  instances. 
It  is  possible  that  some  of  the  cases  of  Landry's  paralysis 
which  have  been  shown  to  be  due  to  peripheral  neuritis, 
were  the  result  of  syphilitic  infection. 

Syphilitic  meningitis,  either  of  the  brain  or  of  the  cord, 
is  not  rarely  associated  with  the  formation  of  gummata. 
In  such  cases  the  symptoms  of  tumor  are  added  to  those 
of  meningitis.  Gummata  may  occur  with  very  little 
meningitis,  and  the  symptoms  of  tumor  then  prepon- 
derate. They  are  much  more  frequent  in  the  brain  than 
in  the  cord. 

The  degenerative  diseases  of  the  nervous  system  stand 
in   an   important   relation   to    syphilis.     None   of  them 


320         DISEASES   OF   THE   NERVOUS   SYSTEM. 

appear  to  be  invariably  due  to  syphilis,  and  some  of 
them  probably  never  are  due  to  it,  but  a  considerable 
number  are  commonly  a  late  sequel  of  syphilitic  infec- 
tion. In  two  important  and  closely  allied  conditions, 
locomotor  ataxia  and  general  paralysis,  a  history  of 
syphilis  can  be  traced  in  seventy-five  or  eighty  per  cent, 
of  the  cases,  and  probably  exists  in  even  a  larger  pro- 
portion. The  various  forms  of  ophthalmoplegia  that 
are  observed  in  tabes  may  occur  as  isolated  conditions 
and  depend  usually  on  syphilis.  The  same  may  be  said 
of  cases  of  simple  atrophy  of  the  optic  nerve,  and  of  the 
rare  cases  of  isolated  Argyll-Robertson  pupil.  Progres- 
sive muscular  atrophy  and  primary  spastic  paraplegia  are 
probably  occasional  consequences  of  syphilis.  In  the  case 
of  ataxic  paraplegia  and  insular  sclerosis,  it  is  very  doubt- 
ful whether  there  is  ever  any  dependence  on  syphilis. 

A  recognition  of  the  various  possible  consequences  to 
the  nervous  system  of  syphilitic  infection  is  often  of  con- 
siderable aid  in  practical  diagnosis.  Having  first  deter- 
mined from  the  character  of  the  symptoms  the  location 
of  the  lesion,  and  from  their  course  its  probable  nature 
(vascular,  inflammatory,  degenerative,  etc.),  we  may  ask 
ourselves,  in  any  given  case,  whether  the  process  that 
has  thus  been  provisionally  diagnosticated  is  one  of  those 
that  may  be  the  result  of  syphilis.  If  the  process  in 
question  may  be  due  to  syphilis,  it  becomes  very  im- 
portant to  know  whether  the  patient  has  a  history  of 
syphilis.  In  a  considerable  number  of  cases  there  has 
been  syphilitic  infection  without  the  knowledge  of  the 
patient,  and  this  is  especially  common  in  women,  in 
whom  the  primary  lesion  is  apt  to  be  overlooked,  and  in 
whom  secondary  symptoms  are  often  slight  or  absent.  As  a 
rule,  in  an  intelligent  person,  who  has  been  infected,  it  is 
not  difficult  to  elicit  a  reasonably  straightforward  history, 


DIAGNOSIS    OF   THE   NATURE    OF   THE   LESION.     32 1 

but,  even  in  such  cases,  slight  symptoms  may  have  passed 
entirely  unnoticed  and  left  no  objective  traces.  It  is 
important,  therefore,  to  realize  the  fact  that  we  can  never 
positively  exclude  syphilis,  unless  we  can  exclude  the 
possibility  of  infection  from  impure  sexual  congress. 
There  are,  however,  many  cases  where  the  possibility  of 
such  infection  cannot  be  excluded,  in  which  the  proba- 
bility of  infection  having  ever  occurred  is  exceedingly 
slight.  When,  in  a  given  case,  there  is  uncertainty  as  to 
past  syphilitic  infection,  to  what  extent  should  this  fact 
be  permitted  to  influence  the  diagnosis  ?  It  is  probable 
that  too  much  weight  is  allowed  to  this  uncertainty.  The 
important  principle  to  bear  in  mind  is  that  any  decided 
indications,  positive  or  negative,  regarding  the  nature  of 
the  lesion,  that  may  be  gathered  from  the  nature  and 
course  of  the  symptoms,  must  be  allowed  full  weight 
even  if  they  are  not  supported  by  what  is  known  or 
believed  regarding  a  history  of  syphilis.  Thus,  if  the 
symptoms  justify  the  belief  that  we  have  to  deal  with  a 
syphilitic  process,  a  process  such  as  rarely  depends  on 
any  other  cause  than  syphilis,  this  belief  should  be 
maintained,  even  if  no  history  of  syphilis  can  be  elicited, 
— unless,  of  course,  the  possibility  of  infection  can  be 
quite  excluded,  which  is  not  commonly  the  case  in 
adults.  On  the  contrary,  if  the  case  is  one  in  which  the 
symptoms  make  a  syphilitic  lesion  unlikely,  this  likeli- 
hood is  not  distinctly  lessened  even  if  it  can  be  shown 
that  the  patient  has  been  infected.  But  if  the  indications 
of  the  nature  of  the  process  as  regards  syphilis  are 
equivocal,  we  must  be  guided  largely  by  the  facts  regard- 
ing the  history  of  syphilis,  and  even  if  these  are  clear 
there  may  remain  a  considerable  chance  for  error. 

There  is  no  satisfactory  proof  that  syphilis    can  ever 
be  looked  upon  as  the  special  cause  of  any  functional 


322         DISEASES   OF   THE   NERVOUS   SYSTEM. 

diseases  of  the  nervous  system.  Even  its  influence  as 
an  indirect  factor  must  be  considered  uncertain.  It  is 
possible,  however,  that  many  morbid  conditions,  both 
organic  and  nutritional,  may  be  remotely  related  to  the 
disease.  The  manner  in  which  organic  changes  in  the 
nervous  system  result  from  syphilis  is  not  fully  under- 
stood ;  in  all  probability  many  of  them  depend  on  the 
action  of  a  toxalbumin,  the  result  of  the  life  processes 
of  micro-organisms,  which  are  with  reason  considered  the 
agents  of  infection  but  about  whose  characters  there  is 
still  no  positive  information. 

Diphtheritic  Infection. — By  far  the  most  frequent  and 
important  organic  disease  of  the  nervous  system  which 
depends  on  the  action  of  the  diphtheritic  poison  is  the 
so-called  diphtheritic  paralysis.  This  paralysis,  which  is 
peculiar  in  distribution  (p.  520),  depends  on  a  lesion  in- 
flammatory in  character  and  limited  mainly  to  the  lower 
or  spino-muscular  segment  of  the  motor  path.  In  some 
cases  both  the  gray  matter  of  the  cord  and  the  peripheral 
nerves  are  involved,  but  in  many  instances  it  is  probable 
that  the  lesion  is  confined  to  the  peripheral  nerves.  It  is 
certain  that  the  peripheral  nerves  are  especially  liable  to 
suffer  from  the  effects  of  the  diphtheritic  poison.  An 
important  peculiarity  of  the  diphtheritic  affection  is  the 
liability  of  the  vagus  nerve  to  be  affected.  The  relation 
between  the  local  affection  in  the  naso-pharynx  and  the 
paralysis  is  usually  obtrusively  clear,  but  it  is  essential 
to  note  that  a  considerable  grade  of  paralysis  may  follow 
a  local  state  so  slight  that  its  diphtheritic  nature  is  over- 
looked. Probably  twenty-five  per  cent,  of  the  cases  of 
diphtheria  that  occur  are  affected  with  some  degree  of 
diphtheritic  paralysis.  A  rare  result  of  diphtheritic  in- 
fection is  hemiplegia  of  sudden  onset,  due  to  one  or  more 
small  hemorrhages  into  the  motor  path.     Such  hemor- 


DIAGNOSIS   OF   THE   NATURE    OF   THE    LESION.     323 

rhages  may  be  so  placed  as  to  cause  no  important  symp- 
toms. A  consequence  of  diphtheria  which  is  of  not  very 
usual  occurrence  is  hysteria.  The  hysterical  symptoms 
may  develop  in  association  with  the  diphtheritic  paralysis, 
or  separately. 

Other  Forms  of  Infectious  Disease. — Tubercular,  syphi- 
litic and  diphtheritic  infection  are,  as  we  have  seen,  ex- 
ceedingly frequent  causes  of  nervous  disease.  Various 
other  infectious  diseases  are  occasional  causes  of  organic 
disease,  and  some  of  them  are  frequent  causes  of  func- 
tional nervous  disease.  The  pathology  of  some  of  these 
conditions  is  as  yet  but  imperfectly  understood.  Among 
the  acute  infectious  diseases  there  is  a  general  correspond- 
ence in  the  clinical  aspects  of  some  of  the  diseases  that 
are  observed.  Thus,  in  the  course  of  any  one  of  the  acute 
infectious  diseases,  symptoms  of  sudden  onset  (hemi- 
plegia, aphasia),  such  as  indicate  a  vascular  lesion  of  the 
brain,  are  liable  to  occur.  In  some  cases  the  lesion  is 
embolism,  in  others  thrombosis  of  an  artery  or  vein,  in 
others  still,  hemorrhage.  Embolism  is  especially  common 
after  scarlatina  and  acute  rheumatism.  These  various 
lesions  are  a  frequent  cause  of  the  acute  cerebral  palsies 
of  childhood.  Convulsions  are  common  at  the  onset  of 
these  processes,  especially  in  children,  where  they  are 
often  indicative  of  cerebral  irritation  only. 

The  other  lesions  dependent  on  infectious  diseases 
present  considerable  diversity  in  character,  and  will  be 
mentioned  in  connection  with  the  diseases  on  which  they 
depend. 

Typhoid  Fever. — Organic  nervous  disease  is  of  much 
less  frequent  occurrence  after  typhoid  fever  than  is  func- 
tional disease.  It  much  more  often  involves  the  cord  or 
peripheral  nerves  than  the  brain.  Paraplegia  of  rapid  or 
subacute  onset  is  occasionally  seen  during  convalescence 


324        DISEASES    OF   THE   NERVOUS   SYSTEM. 

from  typhoid.  It  depends  in  some  cases  on  slight  mye- 
litis, and  in  others  on  multiple  neuritis/  The  paralysis  is 
seldom  complete.  In  rare  cases  the  paralysis  corresponds 
to  the  type  of  acute  ascending  paralysis  (p.  5  24).  In  other 
cases  there  is  localized  atrophic  paralysis  (generally  sub- 
acute) from  poliomyelitis.  Sometimes  there  is  local 
neuritis  of  spinal  nerves,  especially  those  of  the  extremi- 
ties— the  ulnar  and  peroneal  being  those  most  often 
involved.  Sometimes  there  is  paralysis  of  the  palate, 
like  that  which  follows  diphtheria.  Brain  affections  are 
more  rare.  They  include  acute  meningitis  and  hemi- 
plegia (very  rare),  paralysis  of  cranial  nerves,  multiple 
sclerosis,  and  optic  neuritis. 

The  functional  affections  dependent  on  typhoid  fever 
are,  many  of  them,  of  common  occurrence,  and  seem  to 
be  due  to  the  influence  of  a  diffusible  poison  (toxalbumin) 
which  affects  chiefly  the  brain.  Thus  there  are  observed 
bilateral  deafness  (very  common),  loss  of  speech,  not  true 
aphasia  (common);  mental  failure,  as  shown  by  loss  of 
memory,  change  in  character,  or  imbecility;  chronic 
mania;  tremor;  transient  paraplegic  weakness  (very 
common  and  due  perhaps  to  changes  in  the  muscles); 
neuralgic  pains,  and  various  manifestations  of  hysteria 
or  epilepsy  in  those  predisposed  to  these  diseases. 

The  relation  of  these  various  functional  and  organic 
conditions  to  the  preceding  typhoid  fever  is  commonly 
clear  enough.  There  is  nothing  sufficiently  distinctive 
about  any  of  the  conditions  that  have  been  enumerated 
to  enable  one  to  refer  them  to  typhoid  fever  in  the 
absence  of  a  clear  history  of  this  disease. 

'  There  is  but  little  doubt  that  the  neuritis  present  after  many 
cases  of  typhoid  is  due  in  no  small  measure  to  the  indiscriminate  ad- 
ministration of  alcohol  during  the  course  of  the  disease. 


DIAGNOSIS   OF   THE   NATURE    OP^   THE    LESION.     325 

Typhus  Fever  is  only  rarely  the  cause  of  organic  nervous 
affections.  It  is  occasionally  complicated  with  acute 
meningitis,  and  sometimes  followed  by  functional  or  or- 
ganic paraplegia,  as  is  the  case  with  typhoid.  Very  often 
typhus  is  followed  by  optic  neuritis,  probably  not  de- 
pendent on  meningitis.  Functional  disorders  like  those 
following  typhoid  are  not  rarely  observed  after  typhus. 
There  is  nothing  distinctive  about  any  of  the  nervous 
sequelae  of  typhus. 

Scarlet  Fever. — Cerebral  affections  are  more  common 
than  others  from  scarlatina.  The  most  frequent  condition 
is  hemiplegia,  due  in  some  cases  to  embolism  from  endo- 
carditis, in  others  to  thrombosis.  Acute  meningitis  occurs 
with  scarlatina,  but  is  rare.  Convulsions  may  occur  during 
the  disease,  even  when  there  is  no  evidence  of  hemiplegia, 
and  may  persist  in  after  life  as  epilepsy.  Rarely  chorea 
may  occur  as  a  sequela  to  the  disease.  Optic  neuritis 
may  occur  without  symptoms  of  meningitis,  and  without 
evidence  of  nephritis.  Acute  poliomyelitis  occasionally 
appears  to  depend  on  scarlatina. 

Measles. — This  disease  is  an  occasional  cause  of  hemi- 
plegia (from  thrombosis),  and  of  acute  meningitis.  More 
often  it  is  followed  by  spinal  cord  diseases,  of  which  acute 
poliomyelitis  and  acute  myelitis  are  the  most  important. 
In  rare  instances,  measles  has  been  succeeded  by  dissemi- 
nated myelitis,  or  by  acute  ascending  paralysis. 

Small-pox. — Small-pox  is  a  more  frequent  cause  of  acute 
meningitis  than  any  other  eruptive  fever.  Hemiplegia 
as  the  result  of  encephalitis  may  occur.  It  is  also  a 
more  common  cause  of  spinal  cord  disease.  Myelitis, 
especially  the  disseminated  form,  is  perhaps  the  most 
frequent  nervous  lesion.  Poliomyelitis  occasionally  oc- 
curs, and  sometimes  there  is  multiple  or  localized  de- 
generative neuritis.     Acute  ascending  paralysis  has  been 


326        DISEASES   OF   THE   NERVOUS   SYSTEM. 

observed.  Small-pox  has  been  succeeded  by  insular 
sclerosis.  The  ataxia  of  the  arms  and  legs  which  is  now 
and  then  observed  probably  depends  on  multiple  neuritis. 

Erysipelas. — This  disease  is  very  rarely  followed  by 
organic  nervous  disease,  and  some  of"  the  conditions  as- 
cribed to  it  have  probably  depended  on  other  causes. 
Facial  erysipelas  may  cause  unilateral  or  bilateral  paraly- 
sis of  the  facial  nerve,  and  sometimes  results  in  acute 
meningitis. 

Acute  Rheumatism. — The  disease  of  the  nervous  system 
which  most  often  results  from  acute  rheumatism  is  acute 
cerebral  softening  from  embolism,  the  result  of  endo- 
carditis. Spinal  cord  lesions  are  rare.  Myelitis,  how- 
ever, sometimes  occurs,  and  poliomyelitis  has  been  thought 
to  be  frequently  a  consequence  of  acute  rheumatism,  but 
its  occurrence  is  probably  rare.  Multiple  neuritis,  with 
widespread  symptoms,  probably  occurs  in  rare  instances. 

Pneumonia. — Pneumonia  is  a  rare  cause  of  nervous 
disease,  but  is  capable  of  giving  rise  to  various  manifes- 
tations in  different  cases.  The  pathology  and  even  the 
pathological  anatomy  of  most  of  these  morbid  conditions 
is  obscure.  Nervous  complications  and  sequelae  appear 
to  be  most  often  observed  in  cases  of  pneum.onia  that  are 
distinctly  infectious  and  occur  in  epidemics.  This,  as 
well  as  other  facts,  suggests  their  dependence  on  a  micro- 
organism. It  is  probable  that  some  of  the  nervous  lesions 
enumerated  depend  on  the  presence  of  the  Fraenkel- 
Weichselbaum  bacillus,  while  others  depend  on  the  action 
of  a  diffusible  poison  produced  by  this  micro-organism. 
Thus,  purulent  meningitis,  especially  of  the  convexity, 
occasionally  complicates  or  succeeds  pneumonia,  and  is 
probably  due  in  all  cases  to  the  lodgment  of  Fraenkel's 
bacillus  in  the  pia.  Again,  epidemic  cerebro-spinal  men- 
ingitis sometimes  complicates  pneumonia,  and  is  ])robably 


DIAGNOSIS   OF  THE  NATURE   OF   THE   LESION.     327 

due  in  these  cases  to  the  action  of  a  pneumococcus  or 
bacillus. 

Occasionally  pneumonia  is  succeeded  by  symptoms  that 
indicate  a  multiple  neuritis.  These  symptoms  doubtless 
depend  on  the  action  of  a  diffusible  poison.  The  same 
may  be  said  of  the  rare  cases  of  acute  ascending  paralysis 
that  follow  pneumonia. 

Sometimes  nervous  symptoms  suggesting  myelitis  follow 
pneumonia  ;  in  other  cases  there  are  indications  of  mul- 
tiple sclerosis.  Ataxia  of  all  four  extremities  has  been  the 
chief  manifestation,  due  possibly  to  multiple  neuritis. 
Local  paralyses,  with  atrophy  and  altered  sensibility,  are 
occasionally  seen.  In  some  cases  there  have  been  twitch- 
ing of  muscles,  rigidity  of  limbs,  neck,  and  jaw  muscles, 
and  painful  contractions. 

Hemiplegia  during  pneumonia  probably  depends  on 
thrombosis,  determined  often  by  the  existence  of  athe- 
roma. Occasionally  sinus  thrombosis  may  be  caused  by 
extreme  exhaustion,  as  in  other  acute  specific  diseases. 

Influenza — Grippe. — The  epidemic  disease  known  as 
influenza  is  a  far  more  frequent  cause  than  pneumonia 
of  nervous  disorders.  These  are,  however,  for  the  most 
part  functional.  It  is  rare  for  patients  to  recover  from 
this  disease  without  some  functional  nervous  derange- 
ment. Most  often  there  is  a  state  of  neurasthenia  and 
prostration,  sometimes  slight,  but  usually  well  marked, 
and  often  persistent  and  profound.  A  certain  degree  of 
mental  disturbance  is  commonly  linked  with  this  neuras- 
thenic state;  most  often  there  is  slight  mental  depres- 
sion, and  with  this  there  may  be  hypochrondriasis.  In 
those  who  have  mental  disease  all  the  symptoms  are 
exaggerated  by  the  occurrence  of  an  attack  of  influenza. 
Insanity  is  occasionally  caused  by  influenza.  The  follow- 
ing nervous  symptoms  are  met  with  singly,  or  in  combi- 


328         DISEASES   OF   THE   NERVOUS    SYSTEM. 

nation,  during  or  aftfer  the  grippe  :  frontal  headache ; 
dizziness  ;  insomnia  ;  neuro-muscular  pains,  especially  in 
the  back,  calves,  and  thighs  ;  neuralgic  pains  referred  to 
the  eyeballs  ;  paraesthesiae  ;  loss  of  sexual  power  ;  attacks 
of  syncope  ;  tremor  and  unsteadiness  in  gait. 

Organic  disease  appears  to  be  rare  as  a  sequel  of  in- 
fluenza, but  cases  have  been  reported  of  suppurative 
meningitis  and  of  multiple  neuritis.  Spinal  meningitis 
is  probably  sometimes  a  sequel  of  the  disease.  All  these 
conditions,  functional  and  organic,  doubtless  depend  on 
a  diffusible  poison  or  on  a  pathogenic  micro-organism. 

In  many  cases  of  disease  that  unquestionably  depend 
on  infection,  the  source  and  character  of  the  infection  are 
unknown.  Thus,  many  cases  of  poliomyelitis  result  from 
an  unknown  infection.  The  same  may  be  said  of  many 
cases  of  infantile  cerebral  paralyses.  There  is  reason  to 
believe  that  both  these  conditions  may  sometimes  depend 
on  the  same  infection. 

Toxic  Infliie7ices. — We  have  already  passed  in  review 
the  chief  forms  of  infectious  disease  that  give  rise  to 
nervous  disease.  In  so  far  as  these  forms  of  infectious 
disease  produce  their  effects  through  the  agency  of  a 
proteid  substance  derived  from  the  activity  of  living 
micro-organisms,  they  are  to  be  regarded  as  toxic  influ- 
ences. There  remains  for  consideration,  however,  a  class 
of  toxic  influences  very  different  in  character  from  those 
just  mentioned — a  class  of  unorganized  poisons.  This 
class  includes  a  variety  of  organic  and  inorganic  sub- 
stances, many  of  which  are  used  as  drugs.  Of  these,  the 
most  important  in  the  causation  of  organic  nervous  dis- 
eases are  the  heavy  metals,  lead,  arsenic,  mercury  and 
silver,  which  produce  their  most  decided  effect  on  the 
nervous  system  when  taken  into  the  body  in  small  quanti- 
ties and  during  a  considerable  period  of  time.      Many 


DIAGNOSIS   OF   THE   NATURE   OF   THE    LESION.     329 

Other  drugs,  as  quinine,  opium,  belladonna,  strychnine, 
etc.,  produce  nervous  symptoms  when  taken  in  excessive 
doses,  but  are  rarely  productive  of  organic  disease,  and 
do  not  concern  us  here.  Alcohol,  which  is  a  most  im-. 
portant  toxic  agent,  is  considered  elsewhere. 

Lead. — The  entrance  of  lead  into  the  blood  gives  rise  to 
a  variety  of  nervous  disorders.  Chief  among  these  are 
the  clinical  forms  of  disease  that  depend  on  the  action  of 
lead  on  the  lower  segment  of  the  motor  path.  The  prin- 
cipal lesion  resulting  from  lead  poisoning  involves  certain 
peripheral  nerves,  and  especially  the  radial  nerves.  The 
toxic  influence  may,  however,  extend  to  that  portion  of 
the  lower  segment  of  the  motor  path  which  is  located  in 
the  cord,  and  we  may  thus  distinguish  between  the  cases 
of  lead  paralysis  that  depend  on  a  peripheral  degeneration, 
and  those  that  are  due  to  a  peripheral  degeneration  and  a 
degeneration  of  the  ganglion-cells  and  root-fibres  from 
which  the  peripheral  nerves  affected  spring.  The  typical 
symptoms  of  neuritis  from  lead  are  given  elsewhere.  (See 
multiple  neuritis — lead  paralysis.)  A  rare  form  of  lead 
neuritis  causes  laryngeal  palsy. 

In  a  small  number  of  cases  lead  poisoning  gives  rise  to 
cerebral  symptoms.  In  some  of  these  cases  there  are  evi- 
dences of  organic  change  in  the  membranes  of  the  brain  ; 
in  other  cases  there  are  no  alterations,  and  the  symptoms 
appear  to  be  due  to  the  direct  effect  of  the  poison  on  the 
nerve  elements,  which  undergo  nutritional  changes  that 
fall  short  of  structural  alteration.  Among  the  symptoms 
that  arise  in  this  way  are  delirium,  coma,  convulsions, 
and,  occasionally,  hemiplegic  weakness  and  hemianass- 
thesia.  Optic  neuritis  is  an  occasional  but  not  rare  con- 
sequence of  lead  poisoning.  It  is  probably  one  expression 
of  the  direct  action  of  lead  in  the  blood  on  the  peripheral 
nervous  system,  but  it  may  sometimes  depend  on  descend- 


330        DISEASES   OF   THE   NERVOUS   SYSTEM. 

Ing  inflammation  from  the  meninges.  Sometimes  there  are 
the  symptoms  of  an  axial  neuritis — that  is,  scotomata. 

Less  acute  cerebral  symptoms  may  be  due  to  lead. 
Thus,  general  epileptiform  seizures  may  occur  at  inter- 
vals for  a  long  period  after  lead  has  ceased  to  enter  the 
system.  Sometimes  there  is  general  mental  failure,  asso- 
ciated with  general  muscular  weakness.  There  may  be 
melancholia,  with  delusions,  and  in  some  cases  there  are 
symptoms  that  resemble  those  of  general  paralysis  of  the 
insane. 

Severe  abdominal  pain  ("  lead  colic  ")  with  constipa- 
tion are  common  occurrences  when  the  lead  has  entered 
the  system  through  the  intestines.  Pains  in  the  limbs  re- 
ferred to  the  muscles  or  joints  are  common  and  may 
occur  alone  or  in  connection  with  paralytic  symptoms. 
The  pains  sometimes  suggest  a  neuritic  process.  Tremor 
is  an  occasional  occurrence.  It  varies  considerably  in 
character  in  different  cases  and  may  be  associated  with 
paralysis  or  occur  alone. 

An  important  effect  of  lead  is  that  upon  general  nutri- 
tion. A  considerable  degree  of  true  anaemia  is  often 
rapidly  induced  by  the  entrance  of  the  poison  into  the 
circulation.  There  is  also  a  diminution  of  uric  acid  in 
the  urine  and  an  increased  liability  to  the  development  of 
gout.  With  the  liability  to  the  development  of  gout  there 
is  the  strong  liability  to  the  occurrence  of  kidney  disease 
observed  in  gouty  subjects  (chronic  diffuse  nephritis, 
granular  form).  Indeed,  lead  poisoning  may  produce 
kidney  disease  without  inducing  gout.  By  its  coincident 
effect  on  the  heart  and  vessels  lead-poisoning  may  become 
a  cause  of  cerebral  hemorrhage — a  fact  of  considerable 
practical  importance. 

The  extensive  use  of  lead  in  the  industrial  arts  makes 
certain   artisans    particularly    liable    to   lead   poisoning. 


DIAGNOSIS   OF   THE   NATURE   OF   THE   LESION.     33 1 

Plumbers,  painters,  compositors,  and  type-founders  suffer 
most  often.  Painters  constitute  a  large  proportion  of 
cases  of  lead  poisoning.  The  practice  of  "  flatting,"  or 
working  with  lead  and  turpentine  within  doors,  is  par- 
ticularly detrimental.  Those  who  grind  flint  glass  and 
glaze  pottery  sometimes  suffer.  In  many  cases  lead 
enters  the  system  through  what  may  be  called  accidental 
sources,  especially  through  drinking-water  that  has  been 
contaminated  by  lead  pipes  or  cisterns  lined  with  lead. 
An  important  source  of  poisoning  is  from  beer  which  has 
stood  in  lead-lined  receptacles.  Snuff  wrapped  in  lead 
paper  has  been  contaminated,  shot  for  cleaning  demijohns 
has  been  dissolved  in  wine,  etc.,  etc.  Lead  poisoning  has 
resulted  from  the  use  of  lead-containing  cosmetics  and 
hair-dyes,  and  rarely  from  medicinal  preparations,  as 
"  Goulard's  Extract."  It  is  hardly  necessary  to  insist  on 
the  practical  importance  in  diagnosis  of  a  knowledge  of 
the  possible  sources  of  poisoning  when  symptoms  are 
observed  which  may  possibly  be  due  to  lead. 

The  way  by  which  lead  most  frequently  enters  the 
system  is  the  alimentary  canal,  but  it  may  pass  through 
the  skin,  by  way  of  the  nose  (as  in  poisoning  from  snuff 
containing  lead)  and  probably  by  the  lungs.  It  has  been 
thought  that  when  lead  enters  the  system  by  the  skin  it 
may  cause  purely  local  effects  (local  saturnism)  by  purely 
local  action.  It  is  probable  that  local  anaesthesias  are 
sometimes  so  produced,  but  there  is  no  evidence  that 
there  is  ever  muscular  paralysis  from  this  cause. 

The  descendants  of  those  who  have  had  lead  poisoning 
(like  the  descendants  of  alcoholics)  are  especially  liable 
to  develop  functional  nervous  disease  (migraine,  epilepsy, 
neuralgia,  neurasthenia,  chorea,  tic  convulsif,  etc.). 

Arsenic. — The  nervous  symptoms  produced  by  arsenical 
poisoning  bear  a  close   resemblance  to  those  resulting 


332         DISEASES   OF   THE   NERVOUS   SYSTEM. 

from  alcoholic  excess,  and  are  referable,  as  in  alcoholic 
poisoning,  to  a  multiple  neuritis,  or,  more  rarely,  to  mye- 
litis. As  in  neuritis  from  alcohol,  there  are  two  chief 
types  of  arsenical  neuritis, — that  in  which  there  is  paralysis 
of  the  extremities,  and  especially  of  the  extensors  of  the 
hands  and  feet,  and  that  in  which  the  chief  symptom  is 
general  ataxia,  associated  with  diminished  sensibility.  A 
special  variety  of  neuritis,  namely  that  resulting  in  herpes 
zoster,  is  occasionally  a  result  of  arsenical  poisoning. 

Unlike  poisoning  by  lead,  arsenical  poisoning  is  rarely 
dependent  on  occupation,  but  results,  as  a  rule,  from  the 
use  of  pigments  containing  arsenic.  It  may  thus  occur 
from  the  arsenic  contained  in  wall-papers,  in  book  leaves, 
in  artificial  flowers,  and  in  various  paints,  and  enters  the 
system  by  the  lungs.  Sometimes  it  results  from  the 
medicinal  administration  of  arsenic  in  some  form,  par- 
ticularly in  chorea  of  children.  The  quantity  required 
to  produce  toxic  effects  varies  much  in  different  indi- 
viduals. Arsenical  neuritis  may  result  from  the  entrance 
of  small  quantities  of  the  metal  for  long  periods  of  time, 
or  as  a  sequel  of  acute  poisoning,  or  it  may  follow  the 
acute  symptoms  that  sometimes  result  from  the  slow 
accumulation  of  the  metal  in  the  system. 

Mercury — The  nervous  symptoms  that  result  from 
mercurial  poisoning  appear  to  be  chiefly  functional  in 
character  and  of  cerebral  origin.  The  most  important 
symptom  of  mercurial  poisoning  is  a  tremor,  beginning  in 
the  face  and  tongue,  and  extending,  in  time,  to  the  arms 
and  legs, — "  mercurial  tremor,"  or,  in  vulgar  parlance, 
the  "  trembles."  After  a  time  the  tremor  {luide  page  88) 
may  be  associated  with  some  loss  of  muscular  power. 
Other  derangements  may  follow  mercurial  poisoning. 
Of  these  the  chief  are  as  follows  :  neuralgias  (especially 
facial),  formication,  local  partial  analgesias,  mental  irrita- 


DIAGNOSIS   OF   THE   NATURE   OF   THE    LESION.      333 

bility  and  slight  mental  failure,  insomnia,  hallucination 
headache,  irregular  heart  action,  maniacal  excitement.  In 
rare  cases  there  is  aphasia  and  transient  hemiplegic  weak- 
ness. Mercurial  poisoning  is  met  with  chiefly  in  those 
who  work  in  the  metal.  It  is  thus  often  observed  in  quick- 
silver miners,  in  those  who  make  certain  physical  instru- 
ments (barometers,  thermometers),  and  in  those  who 
silver  mirrors.  Less  often  it  is  seen  in  furriers,  hatters,  in 
bronzers,  etc.  The  metal  generally  enters  the  system  by 
the  lungs,  for  it  is  somewhat  volatile  even  at  ordinary  tem- 
peratures. Rarely  it  enters  by  the  skin  or  by  the  alimen- 
tary canal.  Those  who  are  in  depressed  health  are  much 
more  susceptible  than  those  who  are  robust.  It  is  an 
important  practical  point  that  the  symptoms  of  mercurial 
poisoning  may  not  appear  until  some  time  after  the  metal 
has  ceased  to  be  absorbed. 

Silver. — Poisoning  by  silver  has  been  rare  since  the 
practice  of  treating  certain  nervous  diseases  with  salts  of 
silver  has  fallen  into  merited  disuse.  It  almost  never 
results  except  from  the  medicinal  use  of  the  metal.  The 
chief  symptom  of  poisoning  is  a  bluish  discoloration  of 
the  skin  due  to  the  local  deposit  of  silver.  There  is 
often  a  black  line  on  the  gums,  resembling  the  "  lead- 
line." In  very  rare  instances  there  has  been  paralysis  of 
the  limbs  (especially  the  extensors),  dependent,  no  doubt, 
on  neuritis.  The  discoloration  of  the  skin  is  said  to 
begin  when  about  an  ounce  of  the  nitrate  of  silver  has 
been  administered, — no  matter  during  what  period  of 
time  or  in  what  doses. 

It  is  an  important  fact  that  small  doses  of  a  poison 
which  by  themselves  would  give  rise  to  no  toxic  effects, 
are  capable  of  producing  toxic  symptoms  if  these  doses 
act  in  the  presence  of  another  toxic  influence.  Thus  it 
has  been  observed   that  those  who   work  in   the  heavy 


334        DISEASES    OF   THE   NERVOUS    SYSTEM. 

metals  (especially  lead,  arsenic,  mercury,  and  silver)  are 
liable  to  develop  typical  alcoholic  neuritis  from  very 
moderate  indulgence  in  alcohol. 

Trauma. — Traumatic  influences  play  an  exceedingly 
important  role  in  the  production  both  of  organic  and 
functional  nervous  disease.  In  most  of  the  functional 
diseases  related  to  trauma,  the  influence  of  injury  is 
accessory  and  exciting,  and  operates  on  a  predisposition. 
In  many  forms  of  organic  disease  injury  is  the  sole  fac- 
tor. The  character  of  the  injury  varies  as  greatly  in 
different  cases  as  does  the  resulting  form  of  damage. 
The  forms  of  injury  most  often  encountered  are  blows 
and  falls  upon  the  bony  structures  enclosing  the  cerebro- 
spinal axis,  wounds  or  contusions  or  pressure  of  nerve- 
trunks  and  general  concussion.  Upon  the  nervous 
structures  these  traumatic  influences  operate  in  various 
ways  :  by  direct  pressure  on  nerve  elements,  by  pressure 
from  displaced  bone,  by  pressure  from  hemorrhage,  by 
direct  or  indirect  destruction  of  nerve  tissues,  by  causing 
large  or  punctate  hemorrhages  in  or  external  to  the 
nervous  organs,  by  causing  changes  in  the  nutrition  of 
vessels  and  later  in  nervous  elements,  by  exciting  simple 
inflammation,  by  affording  entrance  to  pathogenic  micro- 
organisms, and  by  causing  severe  mental  shock.  Some 
injuries  act  by  several  of  these  mechanisms. 

Some  injuries  give  rise  to  immediate,  or  almost  im- 
mediate, symptoms  ;  others  produce  nervous  symptoms 
only  after  the  lapse  of  time  (days,  weeks,  or  months). 
Of  the  conditions  that  are  the  immediate  consequence 
of  trauma,  some  are  organic,  others  functional.  The 
chief  organic  states  that  are  produced  immediately 
through  trauma  are  as  follows  :  extra-dural  hemorrhage 
(from  middle  meningeal  artery),  with  hemiplegia,  hemi- 
spasm, ptosis,  etc.,  generally  but  not  always  the  conse- 


DIAGNOSIS   OF   THE   NATURE   OF   THE   LESION.     335 

quence  of  fracture  of  the  skull ;  subdural  or  subarachnoid 
hemorrhage,  with  or  without  fracture  ;  laceration  of  brain 
substance,  with  or  without  fracture  (often  opposite  seat  of 
blow)  ;  punctate  hemorrhages  in  the  subcortical  white 
substance  (generally  from  severe  concussion)  ;  subdural 
spinal  hemorrhage,  with  or  without  fracture  ;  hemato- 
myelia ;  complete  or  partial  crush  of  cord  or  cauda 
equina,  from  fracture-dislocation  ;  peripheral  nerve 
paralysis  from  pressure,  laceration,  contusion,  or  section. 
•  The  functional  disturbances  of  the  nervous  system 
immediately  consequent  upon  trauma  are  for  the  most 
part  what  may  be  called  indirect  effects.  Thus,  when 
an  hysterical  paralysis  is  the  immediate  result  of  a  slight 
injury  to  the  part  paralyzed,  the  trauma  operates  through 
the  medium  of  the  cerebrum,  and  not  on  the  part  simply, 
although  the  injury  determines,  at  least  in  a  measure, 
the  part  involved  in  the  paralysis.  In  most  of  the  cases 
of  this  character  there  exists  a  predisposition  (neurotic 
heredity  or  state)  without  which  the  trauma  would  have 
been  quite  inoperative.  Moreover,  there  is  good  reason 
to  believe  that  in  many  cases  of  functional  paralysis  the 
symptoms  are  dependent  largely  on  the  influence  upon 
the  brain  of  accompanying  emotion.  Hence,  the  precise 
role  of  trauma  varies  considerably  in  these  cases  and  is 
not  always  easy  to  define. 

In  a  smaller  class  of  cases  the  influence  of  injury  is 
direct,  as  when  sciatica  follows  directly  upon  pressure 
from  the  edge  of  a  seat.  But  here  again  there  is  often 
a  predisposition  without  which  the  slight  trauma  would 
not  have  become  operative.  Some  cases  of  this  kind  are, 
moreover,  organic,  but  there  is  no  doubt  that  many  of 
them  are  dependent  on  nutritional  changes  solely. 

The  remote  consequences  of  injury — that  is,  those 
which  appear  after  the  lapse  of  days,  weeks,  or  months, 


33^        DISEASES    OF   THE   NERVOUS   SYSTEM. 

are  very  numerous,  and  arise  in  a  variety  of  ways.  We 
may  enumerate  first  the  more  important  organic  states 
that  belong  to  this  category.  It  is  proper  to  include 
here  the  large  class  of  inflammatory  lesions  that  depend 
on  injury :  meningitis,  cerebral  or  spinal,  cerebritis, 
myelitis,  abscess,  neuritis,  arteritis,  etc.  The  develop- 
ment of  new  growths  is  influenced  by  trauma,  but  some 
forms  of  tumor  (using  this  word  in  its  general,  not  in 
its  strictly  pathological  sense),  as  glioma  and  tubercle, 
are  more  often  stimulated  to  activity  through  injury  than' 
the  others.  Cerebral  tumors  are  more  often  related  to 
injury  than  those  which  are  spinal  or  neural.  As  a  class 
the  degenerative  lesions  do  not  appear  to  be  greatly  in- 
fluenced by  trauma,  but  some  forms,  as  tabes,  are  not 
rarely  a  sequel  of  injury.  We  may  inquire  a  little  more 
carefully  into  the  nature  of  the  relation  between  these 
various  classes  of  lesions  and  injuries. 

Trauma  appears  to  give  rise  to  inflammatory  condi- 
tions of  the  nervous  system  in  several  ways.  First,  the 
injury  may  act  on  the  nerve  elements  in  such  a  way  as 
to  cause  their  partial  or  entire  destruction,  with  con- 
sequent inflammatory  infiltration  into  and  about  the 
damaged  parts.  In  this  way  there  may  be  set  up  a 
pachymeningitis,  or  a  neuritis,  or  a  variety  of  other  con- 
ditions. By  this  mechanism  injury  rarely  gives  rise  to 
a  suppurative  process,  but  there  is  little  doubt  that  it 
thus  causes  some  cases  of  acute  myelitis,  and  some  of 
cerebral  abscess.  It  is  possible  that,  in  these  cases,  it 
produces  its  effects  by  the  mechanism  of  severe  concus- 
sion, which  may  cause  extensive  interstital  laceration, 
followed  by  the  local  accumulation  of  immense  numbers 
of  small  spheroidal  cells.  Whether  or  not  in  such  cases 
the  lodgment  of  micro-organisms  is  what  actually 
determines  the   occurrence  of   suppuration   after   such 


DIAGNOSIS    OF   THE   NATURE   OF   THE   LESION.    337 

lacerations,  has  never  been  proven,  but  it  is  in 
accordance  with  the  concepts  of  general  pathology  to 
believe  that  supupration  here,  as  elsewhere,  depends  on 
the  presence  of  micro-organisms.  Without  their  presence 
it  should  seem  that  even  the  most  severe  injury  would 
be  followed  by  an  effort  at  repair.  But  the  most  im- 
portant mechanism  by  which  injury  leads  to  inflamma- 
tion is  of  a  very  different  character  from  those  mentioned, 
and  certainly  depends  on  the  invasion  of  micro-organisms. 
Injury  in  these  cases  affords  to  certain  pathogenic  organ- 
isms an  ingress  to  the  membranes,  or  to  the  nervous 
substance  itself,  or  to  peripheral  nerves.  Thus  after 
fracture  of  the  base  of  the  skull  there  may  be  a  com- 
munication between  the  membranes  and  the  Eustachian 
tube  by  the  tympanum,  through  which  the  pathogenic 
organisms  that  reside  in  the  mouth  i^pneumococcus,  etc.) 
may  pass  and  excite  suppurative  inflammation.  Cere- 
bral abscess  is  often  caused  by  injuries  to  the  head, 
which  open  the  way  to  pyogenic  micro-organisms.  Some- 
times injury  acts  by  giving  rise  to  bone  disease,  which 
in  turn  offers  the  opportunities  for  the  development  of 
inflammatory  processes.  This  is  the  case  with  otitis 
follo\Ying  injury. 

In  its  relations  to  new  growths  in  the  nervous  system, 
trauma  appears  to  act  merely  as  an  excitant,  and  certain 
abnormal  conditions  must  have  pre-existed,  in  a  given 
case,  to  make  trauma  operative,  probably  by  inducing 
changes  both  in  the  structure  and  nutrition  of  the  parts, 
favorable  to  the  development  of  the  variety  of  new 
growth  in  question.  In  no  other  way  is  it  possible  to 
explain  the  influence  of  injury  in  causing  the  develop- 
ment of  infective  granulomata  (syphiloma,  solitary  tuber- 
cle) within  the  nervous  system. 

The  precise  relations  between  injury  and  degenerative 
disease  of  the  nervous  system  are  but  imperfectly  under- 


338        DISEASES   OF  THE   NERVOUS   SYSTEM. 

stood.  In  some  instances  there  is  a  predisposition  to 
such  disease,  as  shown  by  heredity  or  acquired  condi- 
tions, such  as  syphilis  ;  in  other  cases,  as  in  tabes,  no 
predisposition  may  be  recognizable. 

An  important  class  of  remote  effects  of  injury  is  that 
which  includes  the  conditions  known  as  "  traumatic 
neuroses"  (p.  5^8).  The  injuries  in  these  cases  vary 
in  character,  but  are  often  such  as  would  ordinarily  be 
deemed  insignificant.  There  is,  however,  almost  invari- 
ably present  at  the  time  of  injury,  and  consequent  upon 
it,  a  considerable  degree  of  mental  shock,  which  doubtless 
plays  an  important  role  in  the  production  of  the  symp- 
toms. The  traumatic  neuroses  are  commonly  regarded  as 
dependent  on  functional  cerebral  derangements,  but  it  is 
probable  that  in  some  of  the  cases,  at  least,  the  symptoms 
have  been  due  to  slight  but  distinct  organic  changes. 

Injury  to  the  head  is  a  frequent  cause  of  epilepsy. 
Very  often  in  such  cases  it  causes  local  changes  in  the 
pia  and  dura. 

One  of  the  remote  effects  of  injury  (wounds)  to 
which  it  is  necessary  merely  to  allude  here,  is  tetanus. 
This  condition,  like  rabies,  is  dependent  on  the  infection 
of  a  wound,  and  is  considered  elsewhere.  Sometimes 
an  injury  to  the  head  appears  to  determine  the  locality 
in  which  convulsions,  caused  by  a  general  condition 
such  as  uraemia,  repeatedly  take  their  origin.  The 
influence  of  trauma  upon  certain  parts  of  the  nervous 
system  is  distinctly  increased  by  certain  pre-existing 
toxic  influences.  Thus,  pressure  upon  peripheral  nerves 
is  more  effective  in  causing  paralysis  in  those  who  drink 
habitually  to  excess,  or  have  been  poisoned  by  a  metallic 
poison,  or  are  recovering  from  an  infectious  disease, 
than  in  those  who  have  not  been  so  exposed.     The  same 


DIAGNOSIS    OF   THE   NATURE   OF   THE    LESION.      339 

deleterious  influences  render  persons  more  liable  to  the 
development  of  the  traumatic  neuroses  from  slight  in- 
juries. It  has  also  been  noticed  that  alcoholics  and 
convalescents  from  infectious  diseases  are  liable  to  de- 
velop the  symptoms  of  severe  concussion  of  the  brain  in 
consequence  of  slight  head  injuries. 

Reflex  Influences. — The  influence  of  reflex  irritation 
in  causing  nervous  disease  has  been  variously  esti- 
mated. It  has  been  thought  that  many  organic  diseases 
may  at  times  depend  on  reflex  irritation.  Thus  polio- 
myelitis has  been  considered  a  consequence  of  dental 
irritation  in  children,  and  myelitis  of  slight  injury  to  a 
peripheral  nerve  or  of  irritation  from  phimosis.  There 
is  no  evidence  that  organic  disease  ever  depends  on  such 
reflex  influences,  and  their  effect  in  causing  functional 
disturbances  has  certainly  been  much  exaggerated.  In 
almost  all  cases  in  which  peripheral  irritation  appears  to 
cause  functional  diseases  it  acts  merely  as  an  excitant, 
operating  on  a  recognizable  predisposition,  hereditary  or 
acquired.  Thus,  when  attacks  of  migraine  are  deter- 
mined by  strain  of  the  ocular  muscles,  the  underlying 
cause  will  be  found  in  disturbances  of  nutrition  and 
assimilation.  In  a  similar  manner  ocular  strain  may 
result  in  chorea  or  epilepsy,  but  it  is  probable  that  some 
conditions,  as  transient  functional  headache,  may  depend 
solely  on  such  strain.  Of  the  very  numerous  states  that 
have  been  attributed  to  genital  irritation  (paraplegia, 
hemiplegia,  epilepsy,  chorea,  insanity,  etc  ),  none  has 
been  due  solely  to  this  cause.  The  same  may  be  said  of 
the  effects  of  scars,  wounds,  intestinal  worms,  conditions 
of  the  ear,  nasal  defects,  uterine  disease,  etc.  It  is 
probable  that  the  symptom  vertigo  is  often  due  largely 
or  solely  to  the  misleading  sensory  equilibrating  influ- 
ences which  arise  from  the  disturbance  of  certain  special 


340         DISEASES   OF   THE   NERVOUS   SYSTEM. 

sense-organs  (especially  those  of  the  internal  ear),  but 
this  case  is  exceptional  and  does  not  belong  strictly  in 
the  category  of  which  we  are  speaking. 

In  every  case  of  disease  in  which  the  question  of 
causation  by  reflex  irritation  arises,  such  an  origin  should 
not  be  admitted'  until  all  the  more  intelligible  causal 
influences  have  been  excluded. 

Increased  Atmospheric  Pressure  gives  rise  to  one 
important  disease  of  the  nervous  system — namely,  caisson 
paralysis  (see  p.  418).  The  relation  of  this  influence  to 
the  paralysis  in  question  is  usually  obtrusively  evident. 

Exposure  to  Cold. — The  influence  of  no  etiological 
factor  has  been  so  overrated  as  that  of  exposure  to  cold. 
Scarcely  a  form  of  organic  nervous  disease  exists  which 
has  not  at  some  time  been  regarded  as  dependent  on 
cold.  Yet  there  is  no  evidence  that  exposure  to  cold 
ever  acts  except  as  an  excitant,  and  there  is  good  reason 
to  think  that  the  conditions  in  which  it  acts  in  this  way 
are  usually  due  to  some  form  of  infection.  Thus,  though 
poliomyelitis  has  been  considered  due  to  cold,  it  bears 
the  stamp  of  an  infectious  disease,  and  it  is  difficult  to 
see  how  cold  can  do  more  than  determine,  at  times,  the 
occasion  of  its  development.  The  ''  rheumatic  "  oph- 
thalmoplegia of  bygone  days  has  been  shown  to  be  due 
almost  invariably  to  syphilis.  The  most  common  form 
of  facial  paralysis  is  the  so-called  "  rheumatic  "  form, 
which  develops  after  exposure,  often  slight,  to  cold. 
Even  in  this  condition  it  is  possible  that  infection  is 
the  actual  cause  of  the  inflammation,  and  cold  merely 
the  excitant.  And  so  it  is  with  many  other  states, — 
myelitis,  meningitis,  neuritis,  etc.  Belief  in  this  depend- 
ence on  cold  has  been  gradually  shaken  by  the  discovery 
of  more  intelligible  causes.  Many  cases  of  musculo- 
spinal paralysis  were  once  considered  "  rheumatic  "  ; 
they  are  now  known  to  depend  on  pressure. 


DIAGNOSIS   OF   THE   NATURE   OF   THE    LESION.     34I 

When  cold  acts  as  an  excitant  of  disease  it  is  probably 
by  lowering  the  vitality  of  the  parts  concerned.  The 
locus  minoris  resistentiae  may  then  become  open  to  in- 
fluences which  were  before  innocuous.  Such  a  lessening 
of  vitality,  general  or  local,  would  explain  the  increase 
in  the  gravity  of  symptoms  of  organic  disease  which 
sometimes  occurs  after  an  exposure  to  cold. 

Exposure  to  Heat. — Prolonged  exposure  to  heat,  in 
addition  to  giving  rise  to  heat-exhaustion  or  heat-stroke, 
appears  capable  of  determining  the  development  of  in- 
flammatory states  of  the  central  nervous  system.  Thus, 
subacute  poliomyelitis  has  developed  in  adults  from 
unusual  exposure  to  heat.  The  exposure  may  be  to  the 
rays  of  the  sun  or  to  the  heat  of  an  engine-room  or 
kitchen.  Sunstroke  has  been  followed  by  acute  menin- 
gitis. It  seems  to  be  capable  also  of  inducing  the 
symptoms  of  chronic  meningitis.  Sunstroke  has  been 
followed  by  symptoms  resembling  closely  those  of  gen- 
eral paralysis  of  the  insane.  Less  grave  conditions,  such 
as  neuralgias,  irritable  heart  and  various  neurasthenic 
symptoms,  are  a  common  sequel  of  insolation. 

Over-Fatigue  from  Excessive  Exercise. — Over-fatigue 
appears  to  act  as  a  cause  of  nervous  diseases  chiefly 
through  its  temporary  debilitating  effects.  In  this  man- 
ner it  often  determines  attacks  of  neuralgia  or  of  mi- 
graine where  a  predisposition  exists.  Rarely  it  appears 
to  determine  the  development  of  paralysis  agitans.  Some 
cases  of  locomotor  ataxia,  and  others  of  acute  internal 
spinal  meningitis,  appear  to  have  been  related  in  their 
development  to  over-fatigue. 

The  Excessive  Use  of  Particular  Muscles^  or  groups  of 
muscles,  is  a  much  more  important  and  definite  cause  of 
nervous  disease  than  general  over-fatigue.  An  important 
class  of   functional    disorders,  the  occupation  neuroses. 


342         DISEASES    OF   THE   NERVOUS   SYSTEM. 

depends  on  the  habitual  excessive  use  of  particular 
groups  of  muscles.  But  it  is  doubtful  whether  even 
great  excesses  of  this  nature  are  competent  to  bring 
on  these  neuroses  in  the  absence  of  a  central  (cerebral) 
state  of  instability,  shown  not  rarely  by  a  hereditary  ten- 
dency to  functional  nervous  disorders. 

Temporary  paralysis  of  a  part  may  result  from  exces- 
sive use,  and  probably  depends  on  temporary  nutritional 
changes  in  the  anterior  cornual  cells  of  the  spinal  cord. 
Thus,  cases  are  observed  of  paralysis  of  the  lower  ex- 
tremities from  excessive  walking.  Violent  and  excessive 
use  of  muscles  may  lead  to  more  serious  conditions. 
Thus,  spinal  meningeal  hemorrhage  may  occur  at  the 
level  of  the  centres  concerned  in  the  violent  muscular  con- 
tractions, and,  more  rarely,  hematomyelia  results  in  the 
same  way.  In  those  who  have  miliary  aneurisms,  cere- 
bral hemorrhage  sometimes  follows  a  violent  muscular 
effort,  such  as  occurs  in  lifting,  straining  at  stool,  vomit- 
ing and  coughing.  Excessive  use  of  the  muscles  of  the 
legs  appears  to  have  determined  the  occurrence  of  some 
cases  of  acute  myelitis,  and  others  of  acute  poliomyelitis. 
Occasionally  the  symptoms  of  locomotor  ataxia  date  from 
the  excessive  use  of  the  arms  and  legs,  but  it  is  probable 
that  in  these  cases  important  predisposing  conditions  have 
been  present. 

An  important  fact  in  its  diagnostic  bearings  is  the 
occurrence  of  muscular  atrophy  from  the  excessive  use 
of  particular  muscles.  In  engravers,  and  those  who  do 
the  work  of  "  illuminating,"  atrophy  of  the  thenar  emi- 
nence or  of  the  first  dorsal  interosseus  (abductor  in- 
dicis)  is  sometimes  observed.  The  degree  of  atrophy 
may  be  considerable,  but  remains  limited  to  the  muscles 
over-used.  Such  atrophy  probably  never  leads  to  pro- 
gressive muscular  atrophy. 


DIAGNOSIS   OF   THE   NATURE   OF  THE  LESION.     343 

Mental  Shock — Fright. — Of  the  forms  of  mental 
shock  that  influence  the  development  of  nervous  disease, 
the  emotion  of  fright  is  the  most  potent.  Almost  any 
form  of  nutritional  disease  of  the  nervous  system  may 
follow  a  severe  fright,  but  especially  distinct  is  the  rela- 
tion between  fright  and  chorea,  epilepsy,  and  paralysis 
agitans.  When  excited  by  fright  the  conditions  named 
follow  almost  immediately  on  the  event.  Violent  neural- 
gia has  developed  from  fright  and  also  from  grief. 

It  is  a  most  noteworthy  fact  that  violent  fright  appears 
competent  in  rare  cases  to  excite  the  development  of  cer- 
tain forms  of  organic  disease  of  the  brain  in  those  who 
have  appeared,  and  probably  have  been,  quite  free  from 
nervous  disease.  Thus,  organic  vascular  changes  have 
been  found  not  only  in  the  brain,  but  in  the  cord,  in 
cases  of  the  so-called  "traumatic  neurosis"  (p.  538). 
The  influence  of  violent  emotion,  especially  anger,  in  de- 
termining the  occurrence  of  cerebral  hemorrhage  is  well 
known.  Occasionally  emotion  determines  the  occur- 
rence of  cerebral  embolism  in  the  subjects  of  heart  disease. 

Influence  of  Abnormal  Conditio7is  Affecting  the  General 
Health — Cardiac  Disease. — Organic  disease  of  the  heart  is 
of  importance  chiefly  in  its  relation  to  one  process — acute 
cerebral  softening  from  embolism.  The  presence  of 
valvular  disease  of  the  heart  in  a  person  presenting  the 
symptoms  of  acute  cerebral  softening  (p.  553)  is  most  im- 
portant evidence  of  the  nature  of  the  lesion,  provided  the 
other  causes  of  acute  softening  can  be  excluded.  A  con- 
siderable proportion  of  cases  of  chorea  are  preceded  by 
valvular  disease  of  the  heart,  but  the  nature  of  the  rela- 
tion between  these  conditions  is  unknown. 

Feeble  heart-action  is  a  powerful  cause  of  thrombosis 
of  cerebral  vessels,  and  many  of  the  general  causes  of 
thrombosis  (p.  265)  probably  operate  chiefly  through  the 


344        DISEASES   OF   THE  NERVOUS   SYSTEM, 

cardiac  depression  they  cause.  Overaction  of  the  heart 
favors  the  occurrence  of  cerebral  hemorrhage  in  those 
who  have  miliary  aneurisms  of  the  cerebral  vessels. 

Disease  of  the  Vessels. — Of  the  forms  of  arterial  disease 
that  bear  an  important  etiological  relation  to  disease  of 
the  nervous  system,  only  one  form — atheroma — is  recog- 
nizable during  life.  Indications  of  possible  degenerative 
disease  of  the  cerebral  vessels  is  afforded  by  the  presence 
of  atheroma  of  the  accessible  arteries  (radial,  temporal, 
etc.)  and  by  atheroma  of  the  retinal  vessels  (recognizable 
by  means  of  the  ophthalmoscope).  Atheroma  stands  in 
causal  relationship  to  two  conditions  which,  though  very 
different  pathologically,  are  nearly  allied  in  their  clinical 
features — cerebral  hemorrhage  and  acute  softening  from 
thrombosis. 

Kidney  Disease. — Chronic  disease  of  the  kidney,  pri- 
mary or  secondary  to  heart  disease  and  associated  with 
general  arterio-sclerosis  (granular  kidney),  is  an  impor- 
tant cause  both  of  cerebral  hemorrhage  and  of  acute 
softening  from  the  thrombosis  which  occurs  in  atheroma 
of  the  cerebral  vessels.  The  presence,  therefore,  of 
kidney  disease,  does  not  materially  aid  us  in  the  distinc- 
tion of  these  two  forms  of  disease. 

Among  the  nervous  conditions  of  importance  that  are 
met  with  as  a  consequence  of  uraemia,  are  headache, 
insomnia,  stupor  and  convulsions.  The  convulsions  are 
commonly  general,  but  it  is  an  important  fact  that  they 
may  have  a  strictly  local  commencement,  and  may  be  lim- 
ited to  one  side  of  the  body  ;  that  is,  they  sometimes  have 
the  character  of  the  convulsions  so  suggestive  of  a  focal 
brain  lesion.  Optic  neuritis  and  neuro-retinitis  are  not 
rarely  observed  in  the  course  of  chronic  kidney  disease. 

Disorders  of  Digestion  and  Assimilation  are  frequent  and 
potent  causes  of  functional  nervous  derangements,  such 


DIAGNOSIS   OF   THE   NATURE    OF   THE    LESION.     345 

as  headache,  neurasthenia,  mental  depression,  insomnia, 
etc.  Much  remains  to  be  learned  respecting  the  exact 
nature  of  these  nutritional  disturbances,  and  their  rela- 
tions to  special  conditions  and  symptoms.  Organic  dis- 
ease of  the  nervous  system  probably  never  results  directly 
from  such  disorders  of  digestion  and  assimilation. 

Diabetes. — Diabetes  is  often  the  cause  of  continued 
and  severe  headache.  A  more  important  consequence, 
from  a  diagnostic  standpoint,  are  the  convulsive  seizures 
that  are  occasionally  observed  in  the  course  of  the  dis- 
ease. These  are  ordinarily  general,  but  may,  like  the 
seizures  of  uraemia,  be  of  local  commencement.  In  rare 
instances  diabetes  gives  rise  to  a  multiple  neuritis  which 
may  bear  some  resemblance  in  its  symptoms  to  locomotor 
ataxia. 

Rickets^  in  young  children,  is  not  rarely  associated 
with  hydrocephalus.  Rickety  children  often  show  re- 
tardation in  the  development  of  speech.  The  muscular 
weakness  which  is  present  in  these  cases  leads  to  late 
standing  and  walking,  and  may,  in  extreme  cases,  be 
mistaken  for  paralysis.  It  is  not  very  rare  to  see  brief 
attacks  of  loss  of  consciousness,  with  peculiar  reflex 
contraction  of  the  limbs,  in  rickety  young  children. 

Morbid  Blood-States. — Certain  morbid  conditions  of  the 
blood,  such  as  occur  in  acute  diseases,  in  the  terminal 
period  of  cancer  and  tuberculosis,  in  gout,  occasionally 
in  chlorosis,  and  in  various  conditions  of  malnutrition, 
favor  coagulation  of  the  blood  within  the  vessels,  and 
thus  become  an  important  cause  of  thrombosis  of  cere- 
bral vessels.  The  influence  of  these  various  blood-states 
in  causing  thrombosis  is  greatest  in  the  old  and  in  the 
young,  and  in  those  who  have  arterial  disease.  The 
thrombi  of  typhoid  fever  are  due  to  agglutination  rather 
than  coagulation.     The  morbid  blood-state  in  purpura 


34^         DISEASES   OF  THE   NERVOUS   SYSTEM. 

feemorrhagica  may  lead  to  punctate  sub-cortical  hemor- 
iriuges,  but  these  rarely  give  rise  to  symptoms. 

Pregnancy. — The  blood-state  in  the  latter  part  of 
pregnancy  is  such  as  favors  coagulation  of  the  blood 
within  the  cerebral  vessels,  and  hence  it  is  that,  soon 
after  delivery,  the  symptoms  of  thrombosis  of  a  cerebral 
artery  or  vein  are  sometimes  observed  (hemiplegia  of 
sudden  onset,  hemianopsia,  aphasia,  etc).  Exertion  soon 
after  delivery  seems  to  favor  the  occurrence  of  this  con- 
dition. Of  the  functional  states  that  may  arise  from 
pregnancy,  the  chief  are  chorea,  which  usually  develops 
early  (third  month),  and  certain  psychoses  (mania,, 
melancholia). 

Influence  of  Treatment  by  Drugs. — The  only  form 
of  treatment  that  may  afford  an  important  indication  of 
the  nature  of  an  organic  disease  of  the  nervous  system 
is  that  known  as  antisyphilitic.  If,  under  the  influence  of 
antisyphilitic  treatment  (mercury,  potassium  iodide,  sin- 
gly or  together),  there  is  a  rapid  and  considerable  sub- 
sidence of  the  symptoms  due  to  a  lesion  such  as  may 
have  been  caused  by  syphilis  {vide  page  300),  there  is  a. 
considerable  probability  that  the  lesion  was  syphilitic  in 
character,  and  this  probability  may  amount  to  a  practical 
certainty.  If,  on  the  other  hand,  the  symptoms  do  not 
show  considerable  improvement  after  the  administration 
of  maximum  doses  of  iodide  and  mercury  for  a  consider- 
able period  of  time,  there  is  a  considerable  probability 
that  the  lesion  is  not  a  true  syphilitic  lesion.  It  is  very 
important  to  note,  in  this  connection,  that  a  lesion  may 
be  of  syphilitic  origin  and  yet  not  be,  strictly  speaking, 
a  syphilitic  process.  For  example,  acute  cerebral  soft- 
ening occurs  from  syphilitic  endarteritis,  but  there  is 
notJmig  syphilitic  about  the  necrotic  process.  The  softened 
area    has    the    same    pathological   characters    as    soft- 


DIAGNOSIS   OF   THE   NATURE   OF   THE   LESION.     34/ 

ened  areas  from  any  other  cause  of  acute  softening 
(atheroma,  embolism).  The  fact,  therefore,  that  the  soft- 
ening was  due  to  syphilitic  disease  of  an  artery,  renders 
the  necrotic  area  no  more  amenable  to  antisyphilitic 
treatment  than  if  it  had  been  due  to  embolism  or  throm- 
bosis from  atheroma. 

Heredity, — Conditions  of  abnormal  heredity  under- 
lie many  morbid  states  of  the  nervous  system.  In  the 
case  of  some  of  these  morbid  states  the  relation  to  he- 
redity is  uncertain  ;  in  others  it  is  more  definite,  but,  in 
all,  the  ultimate  nature  of  the  relation  is  but  imperfectly 
understood.  For  practical  purposes  it  is  convenient  to 
consider  separately  the  influence  of  heredity  on  mental 
diseases,  on  neuroses  and  on  organic  diseases. 

A  neurotic  heredity  (shown  by  a  disposition  to  func- 
tional nervous  disease  in  the  ancestors)  may  be  traced 
in  the  majority  of  all  cases  of  insanity  but  not  in  all. 
The  graver  chronic  forms  of  insanity,  especially  paranoia, 
and  allied  conditions,  always  develop  on  an  hereditary 
degenerative  basis,  but  the  simple  psychoses,  mania  and 
melancholia,  may  develop  in  persons  without  known 
hereditary  taint.  Very  often  the  heredity  of  insanity  is 
dissimilar  (heterologous) — that  is,  dissimilar  types  of 
disease  develop  in  the  progenitors  and  the  offspring  ; 
less  frequently  the  type  is  the  same,  as  when  paranoinc 
progenitors  have  paranoiac  offspring  or  descendants. 
The  milder  forms  of  mental  disease  often  show  merely 
a  general  neurotic  heredity.  Usually  the  heredity  is 
direct — that  is,  derived  from  parents  and  grandparents  ;; 
less  often  it  comes  from  the  collateral  ancestors  (collat- 
eral heredity). 

Among  the  neuroses  direct  heredity  is  the  rule  and 
similar  heredity  is  common.  Thus,  in  about  two  thirds 
of  the  cases  of  epilepsy  in  which  an  inherited  tendency 


348         DISEASES   OF   THE   NERVOUS   SYSTEM. 

to  the  disease  can  be  traced,  there  has  been  a  family  his- 
tory of  epilepsy.  In  the  remaining  third,  the  inherited 
tendency  was  derived  from  some  form  of  insanity.  But 
a  direct  inherited  tendency  is  shown  in  only  about  one 
third  of  all  cases  of  epilepsy.  In  more  than  half  the 
cases  of  migraine  a  morbid  nervous  heredity  can  be 
shown.  As  a  general  rule  the  inheritance  is  direct  and 
similar — that  is,  the  disease  is  derived  from  a  parent  who 
has  migraine.  In  hysteria  the  influence  of  heredity  is 
much  less  strong  than  in  the  case  either  of  epilepsy  or 
of  migraine  ;  still  it  is  considerable.  The  hereditary  in- 
fluence is  usually  direct  and  maybe  similar  or  dissimilar. 
Hereditary  influence  is  traceable  in  a  small  proportion 
of  cases  (one  sixth)  but  is  very  marked  in  some  of  them. 
The  heredity  is  usually  direct  and  is  often  similar,  but 
may  be  dissimilar  (insanity,  epilepsy).  In  Huntington's 
chorea  the  heredity  is  direct  and  similar  ;  but  it  is  doubt- 
ful whether  this  disease  belongs  in  the  category  of  neu- 
roses. In  paralysis  agitans,  an  hereditary  tendency, 
usually  dissimilar,  and  either  direct  or  indirect,  may  be 
traced  in  a  small  proportion  (about  one  sixth)  of  cases. 
In  exophthalmic  goitre,  in  infantile  eclampsia  (non-symp- 
tomatic), in  tetany,  spasm  of  the  glottis  and  writers' 
cramp,  a  neuropathic  heredity  can  in  many  instances  be 
traced.  But  here,  as  in  the  case  of  the  other  neuroses, 
and  the  psychoses,  the  facts  of  heredity  do  not  afford  us 
material  aid  in  diagnosis. 

Heredity  does  not  appear  to  play  a  very  extensive  role 
in  the  production  of  organic  disease  of  the  nervous  sys- 
tem. Yet,  in  some  cases,  its  effects  are  strikingly  evi- 
dent. An  important  class  of  affections,  the  primary 
myopathies  (p.  453),  show  usually  a  direct  and  similar 
inheritance, — the  transmission  being  most  often  through 
the  mother.     Often  this  influence  extends  through  sev- 


DIAGNOSIS   OF  THE   NATURE   OF   THE   LESION.     349 

eral  generations.  This  is  also  the  case  with  Thomsen's 
disease.  In  pseudo-hypertrophic  paralysis  there  is  often 
a  direct  and  similar  heredity,  but  many  isolated  cases 
occur  and  the  inheritance  may  be  collateral.  It  is, 
however,  almost  invariably  through  the  mother. 

Most  of  the  other  organic  diseases  related  to  a  morbid 
heredity  belong  to  the  degenerative  type  of  nervous  dis- 
eases. It  is  certain  that  some  of  these  conditions,  as 
locomotor  ataxia  and  general  paralysis,  may  depend  on 
hereditary  syphilis,  and  it  is  not  unlikely  that  some  other 
degenerative  diseases,  as  Friedreich's  disease,  maybe,  in 
some  instances  at  least,  the  consequence  of  syphilitic 
taint  in  a  parent — though  at  present  we  have  no  evidence 
that  this  is  so.  The  one  organic  disease  of  the  brain, 
general  paralysis,  which  shows  a  hereditary  influence,  ap- 
pears to  be  related  to  some  form  of  insanity,  or  some 
neurosis  (epilepsy)  in  the  parents,  in  about  37  fo  of  all 
cases.  The  hereditary  influence  is  probably  never  direct 
and  similar — that  is,  general  paralysis  in  the  parent  prob- 
ably never  leads  to  general  paralysis  in  the  offspring. 

A  considerable  number  of  degenerative  diseases  (es- 
pecially those  of  the  cord)  seem  to  depend  on  the  early 
or  late  appearance  of  morbid  structural  characters,  the 
basis  of  which  is  congenital  or  embryonic.  This  is  true 
of  syringomyelia,  hereditary  ataxia,  some  cases  of 
lateral  sclerosis  and  cases  of  arrested  cerebral  develop- 
ment with  mental  defect,  imperfect  power,  inco-ordina- 
tion  and  increased  knee-jerks.  The  character  of  the 
morbid  influences  in  progenitors  that  lead  to  these  con- 
genital states  is  quite  unknown,  but  the  possible  bear- 
ing of  diathetic  conditions,  gout,  diabetes,  syphilis, 
tuberculosis  and  chronic  alcoholism,  should  be  borne  in 
mind. 

With  the  evident  lack  of  accurate  knowledge  respect- 


350         DISEASES   OF  THE  NERVOUS   SYSTEM. 

ing  the  nature  of  hereditary  influences  in  the  production 
of  nervous  disease,  and  the  consequent  inability  to  make 
generalizations,  it  is  not  strange  that  the  diagnostic  indi- 
cations derived  from  heredity  should  be,  as  a  class, 
unimportant.  The  only  exception  to  this  is  in  the  case 
of  the  myopathies  and  Thomsen's  disease,  in  which  the 
usual  family  history  is  of  great  aid  in  fixing  the  nature  of 
the  affection. 

III.  The  Position  of  the  Morbid  Process,  taken 
in  connection  with  the  special  and  known  liability  of 
certain  parts  of  the  nervous  system  to  particular  forms 
of  disease,  is  sometimes  of  considerable  aid  in  the  diag- 
nosis of  the  nature  of  the  lesion.  In  the  case  of  the  brain 
and  spinal  cord,  where  these  indications  are  chiefly  useful, 
they  should  be  employed  in  subordination  to  the  indica- 
tions derived  from  the  mode  of  development  and  the 
causal  factors  that  have  just  been  reviewed.  The  most 
important  facts  to  be  borne  in  mind  in  this  connection 
are  as  follows  : 

In  the  spinal  cord  an  acute  focal  lesion  of  the  white 
substance  is  certainly  inflammatory.  A  focal  lesion  of 
the  gray  matter  is  either  hemorrhage  or  inflammation. 
Lesions  which  affect  definite  systems  of  fibres  in  the 
cord  are  commonly  degenerative  in  character — unless 
they  are  of  acute  or  subacute  onset,  when  they  may  be 
focal  and  consist  of  disseminated  patches  of  inflamma- 
tion^ An  irritative  lesion  of  the  nerve-roots,  if  of 
gradual  development  and  followed  by  symptoms  of  com- 
pression of  nerve-roots,  indicates  compression  of  the 
cord. 

In  the  brain  a  vascular  lesion  of  the  cortex  or  subcor- 
tical region  is  usually  acute  softening,  seldom  hemor- 
rhage. A  vascular  lesion  of  the  pons  or  of  the  medulla, 
which  does  not  cause  death  within  a  few  hours,  is  much 


DIAGNOSIS   OF  THE   NATURE   OF  THE   LESION.     35  r 

more  likely  to  be  acute  softening  than  hemorrhage. 
Obstruction  of  the  basilar  artery  is,  in  the  absence  of 
definite  indications  (as  heart  disease  or  a  history  of 
syphilis),  much  more  likely  to  be  due  to  syphilitic  throm- 
bosis than  to  embolic  occlusion.  This  would  be  true, 
also,  if  equivocal  indications  were  present — such  as  val- 
vular disease  and  a  history  of  syphilis. 

A  lesion  supposed  to  be  tumor  is  likely  to  be  a. 
sarcoma  if  it  begins  outside  the  brain  substance.  A. 
tumor  of  the  cerebral  cortex  is  probably  either  a  glioma, 
or  a  syphiloma.  A  tumor  of  the  cerebellum  or  pons  is 
probably  a  solitary  tubercle  or  a  glioma.  A  tumor  of 
the  crus  is  probably  syphilitic.  At  the  base  of  the  braini 
a  tumor  is  likely  to  be  a  syphiloma,  but  may  be  a. 
sarcoma.  A  basal  tumor,  situated  in  the  position  of  a, 
large  artery,  may  be  thought  to  be  an  aneurism,  provided 
the  patient  is  in  the  second  half  of  life,  has  heart  disease^, 
and  has  had  syphilis,  and  whose  cerebral  symptoms  are 
not  influenced  by  vigorous  antisyphilitic  treatment. 


CHAPTER  V. 

THE    DIAGNOSIS    OF    CLINICAL    TYPES. 

The  first  step  in  the  diagnosis  of  any  case  of  nervous  dis- 
ease  is  to  determine,  at  least  provisionally,  whether  it  be 
of  organic  or  functional  origin,  and  ordinarily  this  is 
readily  done  (see  Chapter  VI.).  If  the  case  appears  to  be 
one  of  organic  disease,  we  endeavor  to  deternmine,  again 
provisionally,  whether  the  morbid  process  affects  chiefly 
the  brain,  the  spinal  cord,  or  the  peripheral  nerves.  The 
value  of  such  a  rough  diagnosis,  when  it  is  possible,  is 
that  it  gives  direction  to  subsequent  efforts  to  make  a 
more  exact  anatomical  and  pathological  diagnosis. 

In  most  instances  a  distinction  between  disease  of  the 
brain  on  the  one  hand,  and  disease  of  the  spinal  cord  or 
peripheral  nerves  on  the  other,  is  a  simple  matter.  The 
distinction  between  spinal  cord  disease  and  peripheral 
nerve  disease  is  usually  easy,  sometimes  difficult,  and 
occasionally  impossible.  The  rough  separation  of  or- 
ganic disease  above  recommended  into  that  of  the  brain, 
cord  and  nerves  is  much  facilitated  by  bearing  in  mind 
the  general  characters  of  disease  in  these  situations. 
These  characters  are  described  in  detail  elsewhere,  but 
they  may  be  advantageously  enumerated  here. 

The  general  characters  of  brain  '  disease  are  as  follows  : 

'  Brain  is  used  to  include  hemispheres,  mid-brain,  cerebellum, 
pons  and  medulla. 

352 


THE    DIAGNOSIS   OF   CLINICAL  TYPES.         353 

1.  Motor,  sensory,  and  trophic  symptoms  are  usually 
unilateral  in  their  distribution.  The  type  of  motor 
paralysis  is  hemiplegic. 

2.  Sensory  symptoms  are  usually  absent  or  slight,  and 
involve  the  distal  portion  of  the  extremities  only.  The 
sensory  changes  are  segmental,  glove,  sleeve,  or  circular 
in  type. 

3.  Trophic  symptoms  are  slight  or  absent.  When 
present  they  are  due  to  non-development  rather  than 
atrophy.  Vaso-motor  symptoms  are  common  and  are 
usually  unilateral. 

4.  Mental  symptoms  are  often  prominent,  and  are 
rarely  entirely  absent.  Loss  of  consciousness, convulsions, 
and  disorders  of  motility  accompany  or  follow  cere- 
bral lesion.  All  disorders  of  motility,  choreiform  move- 
ments, coarse  and  fine  tremors,  etc.,  cease  during  sleep. 

5.  In  functional  brain  affections  the  disorders  of 
movements  are  of  a  unilateral  character,  as  the  move- 
ments of  the  parts  of  one  side  are  more  closely  related 
than  are  the  parts  of  the  upper  or  lower  extremities  of 
both  sides.  The  finer  muscle  movements  are  first  and 
most  affected.  Complex  and  delicate  movements  are 
first  and  most  impaired.  In  convulsive  and  paralytic 
diseases  of  the  brain,  the  arms  are  most  frequently 
affected.  Convulsions  originating  in  the  cerebral  cortex 
are  clonic  in  character. 

6.  The  paralyzed  muscles  never  present  RD. 

7.  The  knee-jerks  are  increased  on  the  paralyzed  side. 
Sometimes  they  are  temporarily  lost  (at  onset  of  acute 
lesions). 

8.  The  sphincters  are  almost  never  paralyzed,  but 
there  may  be  incontinence  from  mental  apathy.' 

^  Occasionally  the  sphincter  ani  is  quite  relaxed,  as  it  is  in  disease 
of  the  lumbar  enlargement,  in  cases  of  sudden  and  complete  hemi- 
plegia.    The  explanation  of  this  is  difficult.     Possibly  it  depends, 
23 


354         DISEASES   OF   THE   NERVOUS   SYSTEM. 

The  general  characters  of  spinal  cord  diseases  are  as 
follows : 

1.  Motor  and  sensory  and  trophic  symptoms  are 
usually  bilateral  and  often  symmetrical  in  their  distribu- 
tion, as  analogous  parts  of  the  upper  or  lower  extremi- 
ties of  the  two  sides  are  closely  related  in  the  cord.  The 
type  of  motor  paralysis  is  usually  paraplegic.  Not  rarely, 
however,  a  small  cord  lesion  produces  strictly  unilateral 
symptoms,  and  then  groups  of  muscles  which  subserve 
definite  acts  are  involved. 

2.  Sensory  symptoms, //" /;-^j^;z/,  are  usually  marked 
(anaesthesia,  analgesia,  etc.). 

3.  Muscular  atrophy  and  other  trophic  symptoms,  if 
present^  are  usually  marked. 

4.  Atrophied  muscles  present  the  RD. 

5.  The  sphincters  are  usually  involved. 

6.  Mental  symptoms  are  absent. 

7.  The  muscle  reflexes  may  be  increased  or  absent  or 
(occasionally)  normal. 

The  general  characters  of  disease  of  the  peripheral 
nerves  may  be  enumerated  as  follows  : 

I.  The  distribution  of  the  motor  symptoms  corre- 
sponds not  to  segments  of  the  body,  as  in  brain  disease, 
nor  to  particular  movements,  as  is  the  case  in  spinal  cord 
disease,  but  to  the  distribution  of  particular  nerves. 
Single  muscles,  or  groups  of  muscles,  corresponding  to 
nerve  distribution  are  involved.' 

like  the  associated  loss  of  knee-jerk  in  such  cases,  on  irritative  in- 
hibition. Similar  relaxation  of  the  sphincter  is  sometimes  observed 
in  CiTUsh  of  the  cervical  region  of  the  spinal  cord. 

'  Occasionally  a  limb  muscle  is  paralyzed  for  one  kind  of  move- 
ment and  not  for  another.  Thus  the  pectoralis  major  may  be  so 
affected  that  it  can  depress  and  adduct,  but  can  no  longer  elevate  the 
arm.     Such  paralysis  of  one  movement  only  of  a  muscle  probably 


THE  DIAGNOSIS  OF  CLINICAL  TYPES.         355 

2.  Sensory  symptoms,  especially  pain,  are  prominent. 

3.  Muscular  atrophy,  if  present,  is  usually  considerable. 

4.  The  atrophied  muscles  usually  present  an  incom- 
plete RD. 

5.  The  sphincters  are  seldom  involved. 

There  are  exceptions,  and  sometimes  important  ex- 
ceptions, to  all  the  rules  formulated  above.  Neverthe- 
less they  hold  good  in  a  large  proportion  of  cases,  and 
are  therefore  useful. 

Clinical  Types  of  Brain  Diseases. 

Meningitis. — The  symptoms  that  indicate  the  exist- 
ence of  acute  meningitis  are  headache,  vomiting,  fever 
and  delirium,  all  of  them  of  rapid  though  not  of  sudden 
onset.  Headache  is  usually  severe,  but  it  varies  in  in- 
tensity at  different  periods  of  the  disease  and  may  be 
absent  at  the  beginning.  It  is  ordinarily  the  most  con- 
spicuous and  persistent  symptom  of  meningitis.  The 
vomiting  of  meningitis  is  often  without  gastric  cause, 
and  may  be  persistent.  It  is  usually  an  early  symptom 
and  is  often  absent  late  in  the  disease.  The  absence  of 
any  one  of  the  four  symptoms  enumerated — headache, 
vomiting,  fever,  delirium — has  little  negative  significance. 
The  mere  combination  of  delirium  and  fever  does  not 
suggest  meningitis.  This  is  an  important  point,  the 
neglect  of  which  leads  to  many  errors  in  diagnosis. 
Besides  these  four  cardinal  symptoms  there  are  other 
symptoms  of  less  constant  occurrence,  the  presence  of 
one  or  more  of  which  adds  to  the  certainty  of  the  diag- 
nosis.    These  are,  rigidity  or  weakness  (often  slight)  of 

always  depends  on  disease  of  the  ganglion-cells  of  the  cord  or  the 
anterior  nerve-roots,  never  on  disease  of  the  peripheral  nerves.  Un- 
fortunately this  point  of  distinction  is  only  rarely  available. 


35t)         DISEASES   OF   THE   NERVOUS   SYSTEM. 

one  or  more  of  the  extremities,  rigidity  of  the  muscles  of 
the  back  of  the  neck,  paralysis  (often  slight)  of  cranial 
nerves,  marked  inequality  or  great  contraction  of  the 
pupils,  strabismus,  convulsions  (local  or  general),  a  slight 
or  considerable  degree  of  optic  neuritis  and  irregular 
respiration.* 

The  existence  of  meningitis  having  been  established, 
or  appearing  highly  probable,  there  remains  to  deter- 
mine, first,  the  situation  of  the  meningitis,  whether  of 
the  base  or  the  convexity,  and  secondly,  the  nature 
of  the  inflammation,  whether  tubercular,  purulent,  or 
simple. 

The  symptoms  which  suggest  Meningitis  of  the  Base 
are  the  early  involvement  (sometimes  extensive)  of  the 
cranial  nerves  (strabismus,  ptosis,  inequality  of  pupils, 
etc.),,  repeated  and  early  vomiting,  the  relatively  late 
occurrence  of  delirium,  the  early  appearance  of  optic 
neuritis,  irregular  breathing  and  rigidity  of  the  muscles 
of  the  back  of  the  neck.  The  most  constant  and  signifi- 
cant of  these  symptoms  of  basal  meningitis  are  early 
palsy  of  cranial  nerves  and  rigidity  of  the  muscles  of  the 
back  of  the  neck. 

On  the  other  hand,  when  delirium  is  pronounced 
and  early,  cranial  nerve  paralyses  are  absent  or  slight, 
and  local  convulsions,  slight  hemiplegia  and  marked 
rigidity  of  the  limbs  occur,  the  indications  point  to  Men- 
ingitis of  the  Convexity.  Infrequent  vomiting  and  the 
absence  of  optic  neuritis  render  a  basal  meningitis  un- 
likely if  the  other  symptoms  are  doubtful  and  if  there 
has  been  time  for  optic  neuritis  to  develop. 

Purulent  Meningitis.     Purulent  cerebral  lepto-meningi- 

'  This  is  a  very  constant  symptom,  especially  in  tubercular  menin- 
gitis, and  should  always  be  looked  for  in  casesof  supposed  meningitis. 


THE  DIAGNOSIS   OF    CLINICAL   TYPES.  35/ 

tis  of  the  convexity  may  be  suspected  if  the  symptoms 
of  acute  meningitis  follow  adjacent  suppuration  or 
a  trauma  or  septicaemia.  The  course  of  the  process  is 
generally  very  acute.  All  of  the  four  cardinal  symp- 
toms of  acute  meningitis — headache,  vomiting,  fever,  and 
delirium — are  usually  well  marked.  The  temperature 
is  commonly  high,  continuous  and  rather  irregular  in  its 
variations.  The  symptoms  vary  in  intensity  in  different 
cases  according  to  the  severity  of  the  process,  and  are 
sometimes  partially  latent  for  a  considerable  period, — 
especially  in  cases  secondary  to  suppuration  in  other 
parts.  The  inflammation  commonly  involves  chiefly  the 
convexity  ;  hence  the  symptoms  are  usually  those  of 
meningitis  of  the  convexity,  but  sometimes  the  process 
extends  to  the  base  and  causes  basal  symptoms. 

Epidemic  Cerebro- Spinal  Meningitis  is  suggested  by  the 
presence   of    symptoms    of    cerebral    meningitis    (basal 
type)   associated   with    those    of  spinal    meningitis,    the 
former  predominating,  and  by  a  very  rapid   and   severe 
onset  of  the  symptoms.     It  is  caused  by  the  diploct)ccus 
intracellularis  of  Weichselbaum.     In  a  typical  case  there 
are  headache,  vomiting,  irregular  and  high  fever,  delirium, 
muscular  rigidity,  general  hypersesthesia  of  the  skin,  and 
retraction  of  the  head.      After  a  time  varying  from  a  day 
to  a  week,  according  to  the   severity    of  the  case,  the 
delirium  that  occurs  in  the  early  stage   of  the  disease 
is  succeeded  by  stupor  deepening  into  coma.     In  some 
cases,  both   severe   and    light,  herpes  labialis   or  herpes 
facialis  makes  its  appearance.     This   eruption   is    com- 
monly an  early  symptom,  and  where  present  is  of  much 
help  in  making  the  diagnosis  of  epidemic  cerebro-spinal 
meningitis.     Petechial  spots  occur  in  a  large  proportion 
of  severe  cases  and  may  also   aid  in   the  diagnosis.     A 
knowledge  of  the  prevalence  of  the  disease  in  epidemic 


358        DISEASES   OF   THE   NERVOUS   SYSTEM. 

form  is  of  great  help  in  distinguishing  between  this  and 
other  forms  of  meningitis. 

Tubercular  Meningitis  ("basal  meningitis")  differs 
somewhat  in  its  symptoms  in  children  and  adults.  The 
symptoms  which  indicate  tubercular  meningitis  in  chil- 
dren are  :  (i)  the  occurrence  for  many  days  and  weeks 
of  a  prodromal  stage,  consisting  of  loss  of  flesh  and 
strength,  and  often  of  slight  irregular  fever,  restlessness, 
irritability,  apathy  and  slight  headache,  followed  by 
(2)  a  period  during  which  these  prodromal  symptoms  con- 
tinue, with  the  addition  of  vomiting  without  gastric  cause 
or  from  inadequate  cause,  and  increased  headache,  fol- 
lowed in  turn  by  (3)  the  symptoms  of  a  /^^i-<7/ meningitis. 
Of  the  symptoms  of  basal  meningitis  {vide  ante)  the  most 
constant  and  significant  in  tubercular  meningitis  are 
retraction  of  the  head,  vomiting,  symptoms  referable  to 
the  cranial  nerves  (especially  strabismus)  and  irregular 
respiration.  The  temperature  is  irregular,  intermittent, 
of  no  special  type,  and  seldom  high.  The  pulse  is  com- 
monly- irregular,  is  infrequent  as  compared  with  the 
respiration  and  not  proportioned  to  the  temperature  ; 
perhaps  it  is  not  only  relatively  but  absolutely  infrequent, 
being  less  than  in  health — 60  to  50,  or  even  40,  per 
minute.  This  is  rather  a  characteristic  symptom.  In 
rare  cases  tubercular  meningitis  involves  only  or  chiefly 
the  convexity,  and  it  must  be  borne  in  mind  that  the 
preponderance  of  the  symptoms  of  convexity  meningitis 
does  not,  in  itself,  exclude  the  possibility  of  the  process 
being  tubercular,  though  it  certainly  creates  a  pre- 
sumption against  this  being  the  case. 

In  adults  the  symptoms  of  tubercular  meningitis  do 
not  differ  essentially  from  those  in  children.  General 
convulsions,  strasbismus  and  retraction  of  the  head  are 
less  common  than  in  children.     Delirium  occurs  earlier 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.         359 

and  headache  is  more  persistent.  In  young  women  hys- 
terical symptoms  may  attend  and  obscure  the  symptoms 
of  the  early  period  of  the  disease. 

Partial  or  Localized  Tubercular  Meningitis  of  the 
convexity  may  produce  focal  symptoms  (local  paralysis 
or  hemiplegia  coming  on  in  the  course  of  a  few  days  or 
weeks,  with  local  convulsions)  much  like  those  of  a 
tubercular  tumor  (see  p.  375).  Such  symptoms  may  be 
combined  with  basal  symptoms. 

Certain  facts  regarding  the  etiology  and  occurrence  of 
tubercular  meningitis  are  of  aid  in  diagnosis.  First,  there 
is  the  fact  that  in  most  cases  there  is  a  family  history  of 
phthisis  or  of  infantile  tuberculosis.  Hence  such  a  history 
in  itself  strongly  suggests  the  tubercular  nature  of  the 
meningitis  in  the  absence  of  other  causes.  Secondly,  in 
adults  the  usual  indications  of  pulmonary  tuberculosis  are 
very  often  present  when  the  meningitis  appears  and  give  a 
clue  to  its  character.  Third,  during  childhood  and  youth 
meningitis  is  far  more  often  tubercular  than  purulent  or 
simple.  Hence  the  mere  circumstance  of  youth  or 
childhood  creates  a  presumption  that  the  inflammation 
is  tubercular. 

Simple^  Non-purulent  Meningitis  (see  page  270)  may 
result  from  trauma,  acute  specific  diseases,  adjacent 
suppuration,  or  from  sunstroke.  It  rarely  or  never  fol- 
lows septicaemia,  and,  with  this  exception,  its  etiology  is 
practically  that  of  purulent  meningitis.  The  symptoms 
of  this  form  of  meningitis  are  essentially  those  of  puru- 
lent meningitis,  generally  with  preponderating  basal  symp- 
toms, but  the  course  of  the  disease  is  usually  somewhat 
longer,  and  the  acute  may  subside  into  a  subacute  stage. 
Simple  meningitis  is  much  more  common  than  the  puru- 
lent form. 

The  diagnosis  of  meningitis  relates  chiefly  to  cases  of 


360        DISEASES   OF   THE   NERVOUS   SYSTEM. 

tubercular  meningitis  since  the  acute  course  and  causal 
relations  of  the  other  varieties  leave  little  room  for  error. 
Lumbar  Puncture  in  the  Diagnosis  of  Menin- 
gitis.— The  diagnosis  of  the  nature  of  an  acute  or  sub- 
acute meningitis  can  often  be  established  with  certainty 
and  facility  by  means  of  evidence  obtained  through  the 
practice  of  lumbar  puncture,  and  this  is  especially  true 
of  epidemic  cerebrospinal  meningitis  and  other  forms 
of  meningitis  in  which  the  spinal  as  well  as  the  cerebral 
meninges  are  the  seat  of  an  inflammatory  process.  The 
presence  of  leucocytes  in  the  fluid  obtained  by  lumbar 
puncture  points  almost  without  exception  to  an  in- 
flammation involving  the  meninges.  The  absence  of  a 
cellular  exudate,  however,  does  not  exclude  meningitis, 
since,  for  example,  it  is  usual  in  tubercular  meningitis 
not  to  find  such  an  exudate.  Much  more  important  is 
the  evidence  derived  from  the  microscopic  and  cultural 
study  of  the  cerebrospinal  fluid.  The  discovery  of  the 
meningococcus  (Weichselbaum's  diplococcus  intracellu- 
laris),  the  pneumococcus,  the  streptococcus  pyogenes,  the 
tubercle  bacillus,  or  other  pathogenic  micro-organism, 
as  the  dominant  or  sole  bacterial  form  in  the  cere- 
brospinal fluid,  fixes  the  nature  of  the  meningitic  pro- 
cess. In  the  case  of  epidemic  cerebrospinal  meningitis 
the  microscopical  examination  is  alone  sufficient  in  most 
instances  to  establish  the  nature  of  the  affection.  In  a 
very  large  proportion  of  cases  of  this  disease  the  menin- 
gococcus is  found  in  the  spinal  fluid  during  the  first  and 
second  weeks  of  the  illness;  the  failure  to  obtain  the 
specific  organism  in  the  second  week  is,  in  the  case  of 
children,  considerably  (though  not  necessarily  absolutely) 
against  the  existence  of  the  epidemic  form  of  cerebro- 
spinal meningitis.  It  must  be  understood  that  symptoms 
indistinguishable   from   those  of   the   epidemic  form  of 


THE   DIAGNOSIS   OF  CLINICAL  TYPES.  361 

cerebrospinal  meningitis  dependent  on  Weichselbaum's 
organism  are  caused  not  very  rarely  by  other  bacterial 
inciters  of  disease,  such  as  the  pneumococcus,  the  micro- 
coccus lanceolatus,  the  streptococcus  pyogenes,  and  the 
tubercle  bacillus. 

The  failure  to  detect  the  tubercle  bacillus  in  the  cere- 
brospinal fluid,  either  on  microscopical  or  cultural  study, 
does  not  exclude  the  possibility  of  tuberculous  menin- 
gitis, since  the  organism  may  be  present  in  very  small 
numbers,  and  animal  inoculation  may  be  necessary  to 
exhibit  its  presence. 

Some  degree  of  prognostic  significance  attaches  to  the 
appearance  of  the  cellular  exudate  in  the  early  stages 
of  acute  cerebrospinal  meningitis  due  to  the  specific 
meningococcus.  The  presence  of  degenerated  leucocytes 
containing  few  micro-organisms,  while  many  cocci  are 
seen  to  be  extracellular,  points  to  feeble  powers  of  re- 
sistance on  the  part  of  the  leucocytes  and  hence  to  a 
bad  prognosis.  On  the  other  hand,  the  presence  of  well 
preserved  leucocytes  showing  many  intracellular  diplo- 
cocci  (indicating  active  phagocytosis)  and  the  absence 
of  many  extracellular  micro-organisms  indicates  good 
powers  of  resistance  and  a  better  prognosis  (other  con- 
ditions being  comparable)  than  in  the  former  case. 

Meningitis  may  be  confounded  (i)  with  other  diseases 
of  the  nervous  system,  and  (2)  with  diseases  outside  the 
nervous  system.  The  following  are  the  conditions  ex- 
ternal to  the  nervous  system  in  which  the  distinction  has 
to  be  made. 

a.  Acute  General  Diseases  (typhoid,  typhus,  etc.). — 
When  a  difiiculty  in  diagnosis  arises  it  is  commonly  in  the 
early  stage  of  these  diseases,  which  are  often  mistaken 
for  meningitis,  though  the  opposite  error  also  is  some- 
times committed.     The  error  is  of  the  same  character  in 


362        DISEASES   OF  THE   NERVOUS   SYSTEM. 

all  the  cases  in  which  an  acute  general  disease  .is  con- 
founded with  meningitis, — the  early  headache,  the  later 
delirium  and  the  fever  are  incorrectly  regarded  as  point- 
ing to  cerebral  disease.  But  the  delirium  of  an  acute 
general  disease  is  always  accounted  for  by  the  fever,  and 
in  the  absence  of  other  symptoms  of  meningitis  (per- 
sistent headache  and  vomiting)  we  are  not  justified  in 
ascribing  the  delirium  to  meningitis  unless  the  tempera- 
ture is  below  101°.  The  headache  of  acute  general  dis- 
eases and  of  febrile  conditions  generally  ceases  when  de- 
lirium cofnes  on  ;  that  of  meningitis  persists.  When  the 
occurrence  of  headache  followed  by  delirium  can  be  ex- 
plained by  the  existence  of  fever  there  is  no  reason  to 
suspect  the  existence  of  meningitis.  Meningitis  should 
be  suspected  in  such  cases  only  when  focal  symptoms, 
such  as  local  spasm  or  paralysis,  or  diffuse  cerebral 
symptoms  which,  like  optic  neuritis  are  not  accompani- 
ments of  general  diseases,  make  their  appearance.  In 
some  instances  a  confident  diagnosis  can  be  made  only 
after  watching  the  course  of  the  symptoms  for  several 
days. 

b.  Intestinal  Disease  in  Children. — In  some  intestinal 
disorders  in  young  children,  especially  exhausting  diar- 
rhoeas, there  may  be  cerebral  symptoms  that  suggest 
meningitis  for  a  time — rigidity,  strabismus,  convulsive 
movements,  somnolence,  and  stupor  and  fever.  The 
diagnosis  is  based  on  the  absence  of  focal  paralytic 
symptoms  and  on  the  short  duration  of  focal  spasmodic 
symptoms — where  these  exist, — the  history  of  intestinal 
derangement,  and  on  the  presence  of  a  depressed  fonta- 
nels. In  rare  cases  intestinal  worms  in  children  give  rise 
to  disordered  nutrition,  irritability,  headache,  rigidity  of 
extremities  and  strabismus,  and  these  symptoms  may  be 
mistaken  for  those  of  tubercular  meningitis.     The  facts 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.         363 

already  given  regarding  tubercular  meningitis  and  the 
diagnosis  of  meningitis  in  general  will  serve  to  prevent 
an  error. 

The  following  are  the  chief  diseases  of  the  nervous 
system  that  are  likely  to  be  confounded  with  meningitis: 

a.  Tumor  of  the  Brain. — A  tumor  of  rapid  growth 
(glioma,  tubercular  tumor)  sometimes  gives  rise  to  symp- 
toms of  rapid  onset  which  may  be  confounded  with  those 
of  meningitis.  Partial  paralysis  of  the  limbs  occurs  in 
both  conditions,  but  in  tumor  it  occurs  early  and  gradu- 
ally, while  in  meningitis  it  is  of  rapid  development  and 
does  not  generally  come  on  early.  The  presence  of 
optic  neuritis  does  not  in  itself  give  any  help,  as  it  may 
occur  in  both  conditions,  but  a  high  grade  of  optic 
neuritis  makes  tumor  highly  probable,  as  does  a  neuritis 
which  develops  rapidly  in  intensity.  The  absence  of 
optic  neuritis  does  not  aid  in  the  diagnosis.  When  no 
indications  can  be  obtained  from  the  focal  symptoms  or 
optic  neuritis,  the  course  of  the  disease  will  often  decide 
the  diagnosis.  If  the  nervous  symptoms  continue  to  in- 
crease for  more  than  a  fortnight  after  the  beginning  of 
the  symptoms  without  the  onset  of  coma  the  case  is  one 
of  tumor  ;  if  the  case  is  one  of  meningitis  the  coma 
will  be  of  earlier  occurrence.  When  meningitis  is  the 
result  of  tumor,  the  symptoms  of  the  tumor  usually  pre- 
cede those  of  the  meningitis,  which  latter  are  distinguish- 
able by  their  acute  onset.  Ordinarily  cerebral  tumors 
cannot  be  confounded  with  acute  or  subacute  menin- 
gitis. The  gradual  onset  and  development  of  the  symp- 
toms and  the  absence  of  fever  in  the  case  of  tumor 
make  the  distinction  from  meningitis,  with  its  more  acute 
onset  and  course  and  its  fever,  sufficiently  easy. 

b.  Abscess  of  the  Brain. — Purulent  meningitis  may  be 
mistaken  for  abscess,  since  the  latter  may  give  rise  to 


364         DISEASES   OF   THE   NERVOUS   SYSTEM. 

symptoms  of  rapid  onset,  and  both  are  often  secondary 
to  the  same  etiological  factors,  injury  and  ear  disease. 
The  course  of  abscess  may  be  latent  until  the  acute 
symptoms  develop,  and  if  these  are  sufficiently  acute  the 
distinction  from  meningitis  may  be  impossible.  More 
often  the  symptoms  of  abscess  run  a  subacute  or  chronic 
course,  and  this  makes  the  distinction  easy  in  most 
instances.  Then  again  the  fact  that  in  meningitis  the 
cranial  nerves  are  more  extensively  and  commonly  in- 
volved than  in  abscess,  helps  in  making  the  distinction. 
The  presence  of  an  active,  persistent,  unilateral  ankle 
clonus  suggests  abscess.  It  must  be  borne  in  mind  that 
purulent  meningitis  is  often  the  terminal  stage  of  abscess, 
and  that  the  two  conditions  may  coexist.  In  such  cases 
the  acute  symptoms  of  meningitis  are  preceded  by  the 
signs  of  more  chronic  cerebral  disease. 

c.  Hysteria. — It  is  not  rare  for  meningitis,  especially 
tuberculous  meningitis,  to  be  mistaken  for  hysteria.  This 
error  is  especially  liable  to  arise  in  cases  of  meningitis 
occurring  in  young  females  who  are  predisposed  to 
hysteria  and  in  whom  hysterical  symptoms  may  appear 
during  the  early  stage  of  the  disease.  Even  if  there  are 
no  actual  hysterical  symptoms  during  the  invasion  of  the 
disease,  a  knowledge  of  previous  hysterical  symptoms  in 
a  young  girl  may  lead  to  the  erroneous  interpretation  of 
the  signs  of  organic  cerebral  disease.  In  cases  where 
doubt  arises  it  may  usually  be  dispelled  by  due  regard  to 
the  temperature,  the  existence  of  local  convulsions  and 
the  state  of  the  fundus  oculi.  Fever,  convulsions  of 
local  commencement  and  optic  neuritis  all  point  strongly 
to  meningitis.  Marked  inequality  of  the  pupils  has  the 
same  significance.  Strabismus  may  occur  in  hysteria  as 
well  as  in  meningitis,  but  is  always  convergent.  Divergent 
strabismus,  therefore,  indicates  meningitis.    In  general  it 


THE   DIAGNOSIS    OF  CLINICAL   TYPES.  365 

may  be  said  that  the  most  important  rule  to  be  followed 
in  doubtful  cases  is  to  look  sedulously  for  any  indications 
whatsoever  of  organic  disease,  and  to  allow  these  their 
full  diagnostic  significance  even  in  the  presence  of  un- 
doubted hysterical  symptoms. 

Chronic  Meningitis. — The  symptoms  of  chronic  menin- 
gitis are  both  focal  and  diffuse,  but  the  focal  symptoms, 
as  paralysis  and  spasm,  usually  predominate.  Fever 
and  delirium,  which  are  commonly  conspicuous  in  acute 
meningitis,  are  absent  or  slight  in  degree  in  the  chronic 
form. 

The  principal  forms  of  chronic  meningitis  met  with  in 
adults  are  the  alcoholic  and  the  syphilitic.  Chronic 
meningitis  in  adults  not  due  to  one  or  both  of  these 
causes  is  exceedingly  rare.  In  children  there  is  a  chronic 
form  of  meningitis  which  is  occasionally  related  to 
syphilis,  but  of  which  the  other  causes  are  unknown. 

Chronic  Alcoholic  Meningitis  is  a  diffuse  process  involv- 
ing chiefly  the  convexity  of  both  hemispheres.  The 
symptoms  are  for  the  most  part  diffuse,  and  consist  of 
headache,  which  is  constant  and  may  be  either  moderate 
or  severe,  mental  dulness  or  apathy  and  sometimes  de- 
lirium. Occasionally  there  is  a  slight  degree  of  optic 
neuritis.  The  disease  runs  an  exceedingly  chronic 
course. 

When  the  symptoms  are  well  developed  the  condition 
is  easy  of  recognition.  The  marked  alcoholic  history,  the 
unmistakable  alcoholic  tremor  and  the  other  evidences 
of  alcoholism  make  plain  the  nature  of  the  diffuse 
cerebral  symptoms.  When  other  and  more  obtrusive 
effects  (such  as  chronic  diffuse  nephritis,  interstitial 
hepatitis,  multiple  neuritis)  of  alcoholism  coexist  with 
chronic  meningitis,  the  symptoms  of  the  latter,  if 
slight,     are     readily    overlooked.       Its     symptoms,    like 


366         DISEASES   OF  THE  NERVOUS   SYSTEM. 

those  of  tumor,  depend  largely  on  the  position  of  the 
lesion. 

Chronic  Syphilitic  Meningitis  is  usually  a  localized, 
seldom  a  diffuse,  process  ;  it  occasionally  exists  where 
there  is  no  distinct  new  growth.  It  occurs,  as  a  rule, 
about  a  syphilitic  growth.  It  may  occur  either  at  the 
base  or  on  the  convexity  of  the  brain,  and  in  either  case 
the  symptoms  are  chiefly  focal  in  character,  and  result, 
from  irritation  and  compression,  especially  from  irrita- 
tion. When  the  meningitis  occurs  about  a  syphilitic 
growth  its  symptoms  are  not  readily  distinguishable 
from  those  of  the  tumor.  When  the  process  exists  alone, 
the  symptoms  still  resemble  those  of  a  syphilitic  tumor, 
with  which  they  maybe  confounded.  As  compared  with 
a  syphiloma,  the  symptoms  of  chronic  syphilitic  menin- 
gitis are  more  irritative  and  less  destructive  in  character. 
When  the  process  involves  the  base  of  the  brain  a  larger 
number  of  cranial  nerves  is  involved  than  is  usual  in 
tumor,  and  the  extent  of  mischief  to  each  nerve  from 
compression  is  less.  The  distinction  of  chronic  syphilitic 
meningitis  from  other  forms  of  chronic  meningitis  is 
based  on  its  limited  extent  and  upon  the  rapid  improve- 
ment that  occurs  on  antisyphilitic  treatment.  The  most 
constant  of  the  diffuse  symptoms  of  chronic  syphilitic 
meningitis  is  headache. 

In  Chronic  Infantile  Meningitis  the  most  constant  and 
distinctive  symptom  is  spasm  of  the  muscles  of  the  back 
of  the  neck,  causing  retraction  of  the  head.  The  develop- 
ment of  this  symptom  may  be  rapid  or  gradual,  and  is 
preceded,  in  some  cases,  by  fever,  repeated  vomiting,  and 
general  convulsions.  There  may  or  may  not  be  rigidity 
of  the  limbs  ;  paralysis  is  rare.  The  symptoms  of  hydro- 
cephalus are  sometimes  added  to  these  symptoms.  Some- 
times retraction  of  the  head  and  convulsions  date  from 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.         367 

birth.  In  these  cases  the  lesion  is  not  meningitis  but 
meningeal  hemorrhage. 

Chronic  infantile  meningitis  may  last  many  months  or 
several  years.  Usually  it  ends  in  death,  but  in  the  cases 
which  depend  on  syphilis  recovery  may  occur. 

Pachymeningitis  Interna  HcBmorrhagica  (Hsematoma 
of  the  dura  mater). — This  is  the  only  form  of  pachy- 
meningitis that  requires  mention.  External  pachymenin- 
gitis is  practically  always  secondary  to  injury  or  to 
neighboring  disease,  and  its  symptoms  are  usually 
obscured  by  those  of  the  primary  trouble.  Purulent 
internal  pachymeningitis,  an  exceedingly  rare  condition, 
gives  symptoms  indistinguishable  from  those  of  purulent 
leptomeningitis. 

Cerebral  Hemorrhage. — It  is  convenient  clinically 
to  divide  all  cases  of  intracranial  hemorrhage  into  two 
groups — of  which  the  first  includes  all  cases  of  hemor- 
rhage into  the  brain  substance — cerebral  hemorrhage 
proper, — while  the  second  includes  all  cases  of  hemor- 
rhage from  the  membranes  of  the  brain — meningeal 
hemorrhage.^ 

The  symptoms  of  cerebral  hemorrhage  proper  vary 
considerably  according  to  the  position  and  size  of  the 
hemorrhage,  but  almost  all  cases  have  certain  features 
in  common — namely  :  i.  The  sudden  onset  of  the 
symptoms.  2.  The  occurrence  of  general  and  usually 
transient  symptoms,  especially  loss  of  consciousness. 
3.  The  occurrence  of  local  and  persistent  symptoms, 
especially  symptoms  of  injury  to  one  motor  tract,  of 
which   hemiplegia   is    the   most  constant  manifestation. 

The  most  common  position,  by  far,  of  hemorrhage 
into  the  brain  substance   is  the  internal  capsule,  and  the 

^  Most  cases  of  hemorrhage  from  meningeal  vessels  are  dependent 
on  injury  to  the  head,  and  are  therefore  treated  elsewhere. 


368         DISEASES   OF   THE   NERVOUS   SYSTEM. 

symptoms  of  capsular  hemorrhage  resemble  those  of 
hemorrhage  anywhere  in  the  motor  tract  of  the  brain, 
and  may  be  regarded  as  constituting  the  type  of  the 
disease.  The  symptoms  that  point  to  a  hemorrhage  in 
the  internal  capsule  are  as  follows  :  i.  Loss  of  con- 
sciousness, of  sudden  or  rapid  onset,  which  is  common 
to  all  cases  in  which  the  hemorrhage  is  large,  without 
reference  to  its  position,  (but  which  maybe  absent  if  the 
lesion  is  very  small)  and  which  presents  the  features  de- 
scribed on  page  184.  2.  Hemiplegia  of  sudden  onset — 
usually  complete — /.  <?.,  involving  face,  arm,  and  leg. 
3.   Motor  aphasia  if  the  hemiplegia   is  on  the  right  side. 

During  the  period  of  unconsciousness,  which  las-ts  in 
those  that  recover  from  a  few  minutes  to  several  hours, 
there  may  be  distinct  evidences  of  a  unilateral  lesion,  as 
unilateral  loss  of  reflex  action,  conjugate  deviation  of  the 
eyes  to  the  side  of  the  lesion,  increased  movement  of  the 
upper  part  of  the  thorax  on  the  paralyzed  side,  defective 
movement  and  flaccidity  of  the  limbs  of  one  side,  etc. 

Some  of  these  symptoms,  such  as  unilateral  loss  of 
reflex  and  conjugate  deviation  of  the  eyes,  wear  away 
soon  after  the  return  of  consciousness.  The  distinctly 
focal  symptoms,  hemiplegia,  and  motor  aphasia,  if  this 
exists,  persist  for  a  variable  period,  according  to  the  ex- 
tent of  the  destruction,  for  the  persistent  focal  symptoms 
depend  on  destruction  of  tissue,  while  the  more  general 
symptoms  depend  on  pressure  and  irritation.  These 
persistent  focal  symptoms  depend  on  the  situation 
of  the  lesion  (see  Localization),  and  constitute  the  most 
important  symptom  of  the  chronic  stage  of  cerebral 
hemorrhage.  The  less  important  symptoms  of  the 
chronic  stage  are  slight  headache  and  some  mental 
change,   very   rarely  convulsions. 

The   symptoms    that    indicate    hemorrhage    in    other 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.  369 

parts  of  the  brain  than  the  internal  capsule  differ  some- 
what from  those  of  capsular  hemorrhage,  according  to 
the  situation  of  the  lesion,  and  may  be  for  the  most  part 
deduced  from  the  account  elsewhere  given  of  cerebral 
localization  (p.  213).  Some  of  these  variations  in  the 
symptoms,  together  with  certain  other  facts  relating 
especially  to  cerebral  hemorrhage,  may  properly  be 
mentioned  here. 

The  symptoms  of  hemorrhage  into  the  substance  of 
the  cortex  differ  from  those  of  hemorrhage  into  the  in- 
ternal capsule  in  the  following  particulars  :  i.  The 
onset  is  generally  attended  by  local  convulsions,  or 
convulsions  having  a  local  commencement.  2.  If  motor 
paralysis  results  it  is  usually  confined  to  one  part  of  a 
side,  face,  arm,  orleg,  after  the  usual  manner  of  cortical 
disease. 

The  symptoms  that  point  to  a  hemorrhage  into  the 
centrum  ovale  closely  resemble  those  of  a  cortical  hemor- 
rhage, without  its  irritative  symptoms.  A  hemorrhage 
into  the  crus  is  indicated  by  crossed  hemiplegia  (see  p. 
224)  with  or  without  hemiansesthesia,  in  addition  tothe 
diffuse  symptoms  of  hemorrhage.  The  symptoms  that  sug- 
gest a  hemorrhage  in  the  pons  are  :  i.  General  convulsions 
attending  the  onset,  or  irregular  convulsions  confined  to 
the  legs.  2.  Bilateral  motor  paralysis.  3.  Marked  bi- 
lateral anaesthesia.  4.  Contraction  or  dilatation  of  the 
pupils.  5.  Respiratory  embarrassment.  6.  Repeated 
vomiting.  7.  High  temperature.  A  hemorrhage  into 
the  medulla,  if  of  considerable  size,  is  rapidly  or  in- 
stantly fatal,  and,  even  if  of  small  size,  is  rarely  survived. 
Cerebellar  hemorrhage  varies  much  in  its  symptoms  (see 
Localization),  and  cannot  ordinarily  be  diagnosed. 
Primary  hemorrhage  into  the  ventricles  can  rarely  be 
diagnosed.  Hemorrhage  into  the  ventricles,  which  is 
secondary  to  hemorrhage  in  other  parts  of  the  brain   is 


370        DISEASES   OF  THE   NERVOUS   SYSTEM. 

suggested  by  :  (i)  the  occurrence  of  a  second  apo- 
plectic seizure  soon  after  the  first,  together  with  (2)  the 
extension  of  hemiplegic  symptoms  (especially  relax- 
ation of  the  muscles)  from  one  side  to  both  sides  of 
the  body. 

Cases  of  hemorrhage  into  the  internal  capsule  makeup 
more  than  one  half  the  cases  of  cerebral  hemorrhage  ; 
next  in  frequency  is  hemorrhage  into  the  centrum  ovale, 
then  in  succession  hemorrhage  into  the  cortex,  pons  and 
cerebellum,  hemorrhage  into  the  medulla  and  cms 
being  very  rare. 

The  most  important  facts  regarding  the  etiology  of 
cerebral  hemorrhage  are,  that  the  disease  is  one  of  the 
second  half  of  life  and  that  chronic  Bright's  disease, 
gout  and  chronic  alcoholism  are  conditions  that  pre- 
dispose strongly  to    its  occurrence. 

The  diagnosis  of  cerebral  hemorrhage  has  to  be  made 
either  during  the  apoplexy,  or  after  the  apoplectic  stage 
has  passed.  During  the  apoplectic  seizure  the  diagnosis 
is  often  difficult  and  occasionally  impossible,  but  it  is 
exceedingly  important  that  every  effort  be  made  to  de- 
termine the  nature  of  the  case,  as  the  correct  treatment 
and  prognosis  depend  upon  it. 

When  a  patient  is  seen  in  apoplexy  and  cerebral 
hemorrhage  is  suspected,  the  first  thing  to  determine  is 
whether  there  are  any  evidences — such  as  hemiplegia,  uni- 
lateral rigidity  or  relaxation,  unilateral  convulsions  or 
unilateral  loss  of  knee-jerk — of  a  focal  brain  lesion.  If  such 
evidences  of  a  sudden  focal  lesion  are  entirely  absent, 
and  if  there  is  no  history  of  unilateral  numbness  or 
weakness  before  the  loss  of  consciousness  came  on,  the 
condition  is  probably  not  dependent  on  a  cerebral 
lesion.  If,  however,  indications  of  a  focal  lesion  are 
detected,  the  dependence  of  the  seizure  on  a  cerebral 
lesion  is  quite  clear.     The  question   to  be  decided  then 


THE   DIAGNOSIS   OF  CLINICAL   TYPES.  371 

is,  is  the  cerebral  lesion  hemorrhage  or  is  it  one  of  the 
varieties  of  acute  softening  ?  The  various  aspects  of  this 
question  are  discussed  under  the  different  forms  of  acute 
softening  of  the  brain.     (See  pages  358,  359,  360.) 

The  apoplectiform  seizures  of  general  paralysis  of  the 
insane  may  be  confounded  with  cerebral  hemorrhage. 
In  the  former,  as  in  the  latter,  there  may  be  sudden  loss 
of  consciousness,  hemiplegia,  unilateral  or  general  con- 
vulsions and  a  rise  in  temperature.  But  in  the  apoplec- 
tiform attack  of  general  paralysis  the  hemiplegia  seldom 
lasts  more  than  a  few  hours,  and  when  the  patient 
comes  out  of  coma  the  distinctive  mental  and  physical 
indications  of  the  disease  become  only  too  evident. 

Sudden  apoplectic  seizures  not  due  to  a  cerebral 
lesion,*  of  short  duration  and  usually  without  any  local 
symptoms,  but  sometimes  accompanied,  by  slight  and 
transient  hemiplegic  weakness,  are  occasionally  observed 
These  seizures  occur  in  elderly  persons,  and  may  be 
mistaken  *  for  cerebral  hemorrhage.  In  a  first  attack 
the  distinction  may  be  impossible.  The  diagnosis  is 
based  on  the  absence  of  deep  coma  and  the  absence 
or  transient  duration  of  focal  symptoms.  Sometimes  a 
history  of  repeated  attacks  of  this  character  can  be 
obtained,  and  this  is  a  great  aid  in  the  diagnosis.  The 
nature  of  these  seizures  is  unknown.  They  have  been 
thought  to  depend  on  cerebral  *'  congestion,"  and  it 
may  be  that  some  of  the  cases  are  of  this  nature  ;  but 
it  is  probable  that  in  some  cases,  at  least,  the  symptoms 
depend  on  diminished  blood-supply  to  motor  structures 
of  the  brain,  due  to  transient  spasm  of  cerebral  arteries. 

Acute  Cerebral  Softening   (Softening  from  Arte- 
rial Occlusion,  Necrotic  Softening,  Encephalomalacia.) — 

^  In  numerous  cases  of  this  kind  the  patient  has  died  from  other 
causes  and  the  autopsy  has  failed  to  show  any  lesion. 


IJ2         DISEASES   OF   THE   NERVOUS   SYSTEM. 

The  symptoms  that  characterize  acute  cerebral  soften- 
ing closely  resemble,  in  their  general  features  and  in 
many  details,  the  symptoms  that  result  from  cerebral 
hemorrhage  (see  p.  348). 

As  in  hemorrhage  there  are  :  (i)  general  and  transient 
symptoms  (as  loss  of  consciousness)  due  to  general  dis- 
turbance of  brain  function  ;  (2)  local  and  enduring 
symptoms  (especially  hemiplegia,  and  when  the  lesion  is 
on  the  left  side,  motor  aphasia)  dependent  on  the  situa- 
tion of  the  lesion,  and  due  directly  to  the  destruction  of 
tissue  caused  by  it  ;  and  (3)  these  symptoms  are  usually 
either  of  sudden  or  of  rapid  onset. 

In  addition  to  this  general  resemblance  between  acute 
softening  and  hemorrhage  there  is  a  resemblance  in  de- 
tails between  certain  forms  of  softening  and  hemorrhage 
that  would  make  the  two  indistinguishable  more  often 
than  they  are,  were  it  not  for  the  diagnostic  aid  derived 
from  the  study  of  the  causal  indications. 

Two  principal  forms  of  acute  softening,  based  on 
pathological  differences  (see  page  264)  must  be  dis- 
tinguished. These  are  :  (i)  softening  from  embolism  and 
(2)  softening  from  thrombosis.  The  latter  form  includes 
three  sub-varieties  :  (i)  Thrombosis  from  atheroma, 
(2)  from  syphilis,  and  (3)  from  blood  states,  between 
which  it  is  important  to  distinguish  clinically.  These 
different  forms  of  acute  softening  from  arterial  obstruc- 
tion make  up  a  large  and  important  group  of  cases  ; 
they  are,  in  fact,  as  common  if  not  more  common  than 
cases  of  cerebral  hemorrhage. 

Acute  Softening  from  Embolism. — In  acute  softening 
from  embolism  premonitory  symptoms  are  exceedingly 
rare  ;  the  onset  is  sudden,  the  loss  of  consciousness  and 
the  accompanying  focal  symptoms  coming  on  in  the 
course    of    a  few    seconds   or    minutes.     In    rare    cases 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.         373 

the  onset  is  gradual,  occupying  several  hours,  and  in 
these  cases  there  may  be  no  loss  of  consciousness.  As  a 
rule,  the  more  acute  the  onset  the  greater  the  likelihood 
of  there  being  loss  of  consciousness,  but  this  is  of  short 
duration  in  embolism.  Convulsions  are  also  frequent  in 
embolism,  at  the  onset  ;  they  may  be  general  or  local. 
When  the  beginning  is  local  it  is  generally  in  the  part 
afterwards  most  paralyzed.  The  focal  symptoms  are  like 
those  of  hemorrhage  and  vary  similarly  with  the  position 
of  the  lesion.  Hemiplegia  is  a  very  constant  symptom. 
Partial  hemiplegia,  especially  paralysis  of  the  arm,  or  of 
the  face  and  arm,  is  not  uncommon.  It  is  much  more 
frequent  than  in  hemorrhage.  When  the  lesion  is  on 
the  left  side   aphasia  is  as  common  as  in  hemorrhage. 

The  etiological  facts  regarding  embolism  which  it  is 
important  to  remember  are  : 

a.  That  there  is  usually  present,  at  least  during  the 
first  year  after  the  onset  of  the  symptoms  of  embolism, 
distinct  indications  of  valvular  disease  of  the  heart 
(especially  mitral  stenosis). 

b.  That  the  absence  of  evidences  of  endocarditis  a 
year  or  more  after  the  onset  is  perfectly  consistent  with 
the  occurrence  of  embolism,  provided  the  onset  suc- 
ceeded a  disease  which,  like  scarlet  fever,  chorea  or 
rheumatism,  is  apt  to  be  associated  with  valvular 
disease. 

c.  That  embolism  occurs  most  frequently  during  later 
childhood  and  early  adult  life,  though  it  may  occur  at 
any  period  of  life. 

Acute  Softening  from  Syphilitic  Thrombosis  {i.  e.,  from 
syphilitic  endarteritis). — The  symptoms  of  acute  soften- 
ing from  syphilitic  thrombosis  usually  differ  in  several 
respects  from  those  of  embolism.  First,  premonitory 
symptoms   are   the   rule.     The  attack  is  preceded  very 


374         DISEASES   OF   THE   NERVOUS    SYSTEM. 

often  by  well  marked  cerebral  symptoms.  Of  these 
headache  is  the  most  common  and  characteristic.  The 
headache  is  frequently  severe  and  is  often  aggravated 
at  night.  Other  less  constant  premonitory  symptoms 
are  giddiness,  mental  apathy  or  somnolence,  numbness 
of  one  or  more  extremities  and  slight  hemiplegic  weak- 
ness. Another  point  of  difference  is  that  in  syphilitic 
thrombosis  loss  of  consciousness  at  the  onset  is  much 
more  common  than  in  embolism,  being  absent  in  about 
half  the  cases.  Initial  convulsions  are  also  much  more 
rare.  The  focal  symptoms  present  no  important  points 
of  difference. 

The  etiological  facts  bearing  on  the  diagnosis  of  syphi- 
litic softening  which  it  is  important  to  bear  in  mind  are  : 

a.  That  there  is  a  history  of  syphilitic  infection  in  a 
large  number  of  cases,  and  that  the  date  of  this  infection 
varies  from  a  year  to  twelve  or  fifteen  years  before  the 
onset  of  the  symptoms  of  softening. 

b.  That  in  the  cases  where  a  history  of  syphilis  can- 
not be  obtained  (as  in  coma),  but  where  infection  cannot 
be  positively  excluded,  reliance  must  be  placed  on  the 
age  of  the  patient  and  on  the  absence  of  other  causes 
(atheroma,  blood  states)  of  acute  softening.  The  import- 
ant fact  regarding  age  is  that  softening  from  syphilis  is 
rare  before  twenty  and  after  fifty  and  that  half  the  cases 
occur  between  the  thirtieth  and  fortieth  year. 

Acute  Softening  from  Atheroma. — The  symptoms  of 
softening  from  atheroma  do  not  differ  essentially  from 
those  of  softening  from  syphilitic  endarteritis  ;  as  com- 
pared with  embolism  there  is  the  same  frequency  of 
premonitory  symptoms  '  (especially  slight  general  head- 

^  It  is  of  course  very  evident  why  premonitory  symptoms  are 
absent  in  softening  from  embolism  and  usually  present  in  softening 
from  atheroma  and  syphilitic  endarteritis.  In  the  case  of  softening 
from  atheroma  or  syphilitic  endarteritis  the  arterial  disease  gradually 


THE   DIAGNOSIS   OF    CLINICAL    TYPES.  375 

ache,  numbness,  hemiplegic  weakness  and  slight  mental 
change),  and  a  similar  though  not  equally  marked  im- 
munity from  loss  of  consciousness  in  some  cases.  The 
similarity  in  symptoms  extends  to  the  focal  as  well  as  to 
the  diffuse  symptoms.  The  etiological  facts  relative  to 
the  diagnosis  are  as  follows  : 

a.  Softening  from  atheroma  is  chiefly  a  disease  of  the 
second  half  of  life.  Before  the  age  of  forty  it  is  infre- 
quent except  in  association  with  chronic  Bright's  disease 
(chronic  diffuse  nephritis).  After  forty  the  liability  to  the 
disease  increases  as  life  advances,  and  this  liability  con- 
tinues to  increase  until  extreme  old  age.  Senility  is 
therefore  a  most  important  etiological  factor. 

b.  Chronic  alcoholism  predisposes  to  atheroma,  and 
any  condition  which,  like  blood  disease  or  cachexia, 
favors  thrombosis,  favors  softening  from  atheroma.  The 
occurrence  of  atheroma  of  the  vessels  of  the  brain  is 
favored  by  injury  to  the  head. 

Acute  Softening  from  Blood-States  (Simple  Arterial 
Thrombosis). — Arterial  thrombosis  from  a  blood-state 
alone,  without  the  existence  of  arterial  disease,  is  a  rare 
cause  of  acute  softening  of  the  brain.  It  usually  results 
in  adults  from  the  state  of  the  blood  that  exists  during 

diminishes  the  lumen  of  the  diseased  vessels,  and  a  point  is  at  length 
reached  where  the  quantity  of  blood  passing  through  the  vessel  is  so 
little  as  to  i?npair  the  nutrition  of  the  parts  supplied  by  it  without 
destroying  them.  This  is  the  period  of  premonitory  symptoms.  The 
diminished  blood-stream  favors  coagulation,  and  after  a  variable 
period  a  thrombus  forms  at  the  highly  diseased  region  of  the  vessel. 
The  blood  supply  of  the  dependent  parts  is  then  suddenly  shut  off, 
with  resulting  softening  of  these  parts  and  loss  of  consciousness, 
hemiplegia,  etc.  In  softening  from  embolism,  on  the  contrary,  the 
sudden  lodgment  of  the  embolus  is  not  preceded  by  any  vascular  dis- 
turbance, the  impairment  in  nutrition  of  the  brain,  is  sudden  and 
great  and  the  symptoms  are  of  sudden  onset  and  without  premonitions. 


376         DISEASES   OF   THE    NERVOUS    SYSTEM. 

the  puerperal  state,  and  the  indications  of  the  cause  are 
always  evident  and  usually  obtrusive.  The  symptoms  in 
such  cases  resemble  those  of  embolism,  the  focal  symp- 
toms varying  similarly  with  the  position  of  the  lesion. 

When  a  blood-state  like  that  which  accompanies 
tuberculosis,  cancer,  acute  diseases,  etc.,  is  associated 
with  disease  of  the  cerebral  arteries,  it  has  an  important  in- 
fluence in  favoring  the  occurrence  of  thrombosis  in  them. 

The  occurrence  of  softening  from  an  arterial  obstruc- 
tion should  be  suspected  in  cases  giving  a  history  of  a  sud- 
den cerebral  lesion  in  the  presence  of  conditions  that  are 
recognized  as  the  causes  of  such  arterial  obstruction. 
The  diagnosis  of  the  cause  of  the  softening  (embolism, 
syphilitic  endarteritis,  atheroma,  blood-state)  depends 
on  the  causal  indications^  and  in  far  slighter  degree  on 
the  character  of  the  symptoms  that  point  to  the  sudden 
cerebral  lesion.  These  various  indications  have  been 
already  sufficiently  considered.  The  chief  diagnostic 
problem  relating  to  acute  softening  is  the  distinction 
from  cerebral  hemorrhage.'  The  form  of  acute  soften- 
ing which  it  is  most  difficult  to  diagnose  from  hemor- 
rhage is  that  from  atheroma.  The  diagnosis  between 
embolic  softening  and  hemorrhage,  and  between  syphi- 
litic softening  and  hemorrhage,  is  rendered  much  simpler 
by  the  etiological  indications. 

I.  The  Diagnosis  between  Softening  from  Atheroma 
and  Cerebral  Hemorrhage  can  be  made  with  a  high  de- 
gree of  probability  in  a  considerable  number  of  cases, 
but  is  impossible  in  others.  In  all  cases  it  is  a  matter 
of  probability,  and  that  is  more  often  low  than  high. 
In  every   case  where  the  question  of  such  a  diagnosis 

'  This  is  an  exceedingly  important  question  to  decide,  on  account 
of  its  bearing  upon  treatment,  which  in  the  one  case  is  stimulating 
and  in  the  other  is  depressing  to  the  heart. 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.  377 

arises  a  conclusion  should  be  reached  only  after  a  care- 
ful study  of  all  the  symptoms,  both  general  and  focal, 
and  of  the  causal  indications.  The  following  are  the 
more  important  symptomatic  and  causal  indications  : 

Prodromic  symptoms  {vide  atheroma),  if  present,  point  to 
softening,  but  their  absence  does  not  point  to  hemorrhage. 

Little  help  is  to  be  derived  from  the  degree,  duration 
and  occurrence  of  loss  of  consciousness,  unless  there  is 
some  indication  of  the  size  of  the  lesion.  If  the  lesion 
is  probably  small  (as  indicated  by  partial  hemiplegia), 
loss  of  consciousness  is  decidedly  in  favor  of  hemor- 
rhage. If  the  lesion  is  probably  large,  the  absence  of 
loss  of  consciousness  points  strongly  to  softening.  In 
the  absence  of  indications  relating  to  the  size  of  the 
lesion  deep  coma  makes  hemorrhage  probable,  while  a 
slight  attack  of  apoplexy  of  transient  duration  is  in 
favor  of  softening.  A  general  convulsion  at  the  com- 
mencement of  the  attack  makes  hemorrhage  more  likely, 
but  initial  local  spasm  points  to  softening. 

If  the  temperature  falls  more  than  one  degree  at  the 
time  of  the  onset,  or  if  it  rises  several  degrees  within 
a  few  hours  after  the  onset,  this  is  much  in  favor  of 
hemorrhage,  except  in  cases  where  the  lesion  is  situated 
in  the  pons,  when  the  rule  loses  its  value. 

When  the  early  stage  is  past  the  repeated  occurrence 
of  convulsions  commencing  in  the  paralyzed  extremities, 
and  the  presence  of  athetoid  moveiJients  or  post-hemi- 
plegic  agitation  or  tremor  indicate  that  the  lesion  was 
softening,  not  hemorrhage.  Of  the  causal  indications,  the 
condition  of  the  heart  and  arteries  is  the  most  important. 
High  arterial  tension  and  a  bounding  pulse  at  the  time  of 
the  attack  point  to  hemorrhage  if  the  other  indications 
are  balanced,  while  a  feeble  and  irregular  pulse,  especially 
if  compressible,  suggests  softening.   As  the  conditions  of 


378        DISEASES   OF  THE   NERVOUS   SYSTEM. 

disease  observed  in  association  with  hemorrhage  and 
softening  from  atheroma  are  much  the  same,  their  value 
in  this  diagnostic  problem  is  limited.  A  considerable 
degree  of  atheroma  of  the  arteries  points  to  softening 
rather  than  hemorrhage,  but  only  if  the  other  indications 
are  equal.  The  reverse  is  true  of  an  advanced  state  of 
chronic  diffuse  nephritis.  A  history  of  a  cachexia  or  an 
exhausting  illness  before  the  onset  favors  softening. 
The  age  of  the  patient  does  not  help  much,  but  the 
greater  the  age  above  seventy-five  the  greater  are  the 
chances  that  the  process  is  softening,  while  under  forty- 
five  hemorrhage  is  more  probable. 

2.  The  Diagnosis  between  Softening  frofn  Syphilitic 
Endarteritis  and  Cerebral  Hemorrhage  is  ordinarily  a  less 
difficult  problem  than  the  one  just  described,  and  in  it 
the  causal  indications  play  a  more  important  role.  The 
important  differential  points  are  the  following  : 

The  presence  of  prodromata  indicate  softening,  but 
their  absence  does  not  aid  in  the  diagnosis.  The  facts 
relating  to  loss  of  consciousness  are  the  same  as  in  the 
diagnosis  between  softening  from  atheroma  and  hemor- 
rhage (vide  ante).  A  history  of  acquired  syphilis,  if  the 
other  indications  are  balanced,  makes  softening  very 
probable,  but  if  there  is  reason  to  suspect  that  the  leaion 
is  hemorrhage,  a  specific  history  does  not  render  this 
diagnosis  improbable,  since  syphilis  may  lead  to  hemor- 
rhage by  causing  an  aneurism.  But  if  there  is  a  history 
of  syphilis  in  a  patient  over  fifty  this  has  little  signifi- 
cance in  favor  of  softening.  The  presence  of  atheroma 
or  chronic  Bright's  disease  makes  the  diagnosis  of  hem- 
orrhage highly  probable,  as  between  hemorrhage  and 
softening  from  syphilitic  disease.  The  absence  of  athe- 
roma and  chronic  Bright's  disease,  with  a  possibility  of 
syphilitic  infection,  suggests  softening.     The  age  of  the 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.         379 

patient  generally  gives  important  help  in  the  diagnosis, 
since  before  the  age  of  forty  the  chances  are  much  in 
favor  of  syphilitic  softening,  and  after  forty-five  they 
are  equally  in  favor  of  hemorrhage.  If  the  patient  is 
between  forty  and  forty-five  years  of  age  the  indications 
derived  from  age  are  of  no  value. 

3.  The  Diagnosis  between  Softening  from  Embolism  and 
Cerebral  Hemorrhage  ordinarily  presents  few  difficul- 
ties. Deep  prolonged  coma  is  strongly  in  favor  of 
hemorrhage  ;  the  absence  of  loss  of  consciousness,  or  a 
slight  and  temporary  loss  of  consciousness,  suggests  em- 
bolism. The  most  important  evidences  in  favor  of  em- 
bolism are  the  presence  of  a  cause  of  embolism  (heart 
disease,  aneurism)  in  a  patient  under  forty  years  of  age. 
If  the  patient  is  between  forty  and  fifty  embolism  is 
still  probable,  if  there  is  a  cause  of  embolism,  but  after 
this  period  becomes  improbable.  It  is  often  stated  that 
the  presence  of  right  hemiplegia  is  a  point  in  favor  of 
embolism,  but  this  is  an  error.*  In  rare  instances  the 
diagnosis  of  embolism  may  be  made  through  evidences 
of  an  embolic  process  in  another  part  of  the  body. 
Thus,  the  occurrence  of  an  infarction  of  the  spleen,  as 
shown  by  tenderness  and  enlargement  coming  on  acutely, 
or  the  occurrence  of  obstruction  of  the  central  artery  of 
the  retina,  as  shown  by  ophthalmoscopic  changes,  about 
the  time  of  a  sudden  cerebral  lesion,  make  the  existence 
of  cerebral  embolism  in  the  former  case  exceedingly 
probable,  and  in  the  latter  practically  certain. 

Meningeal     Hemorrhage. — Only    two    forms    of 

'  Right  hemiplegia  from  embolism  is  certainly  rather  more  com- 
mon than  left  hemiplegia  (about  6-5),  but  the  difference  in  the  inci- 
dence of  the  hemiplegia  is  not  enough  to  constitute  a  diagnostic  sign, 
and  would  not  constitute  a  valuable  sign  if  the  difference  were  much 
greater. 


380         DISEASES   OF   TEIE    NERVOUS   SYSTEM. 

meningeal  hemorrhage,  both  of  them  dependent  upon  in- 
jury, require  our  notice.  Of  these  two  forms,  one — in- 
fantile meningeal  hemorrhage — occurs  in  the  course  of 
delivery,  and  is  the  cause  of  an  important  form  of  in- 
fantile cerebral  palsy  (see  p.  367).  The  hemorrhage  in 
these  cases  is  between  the  dura  and  pia  over  the  con- 
vexity, usually  on  one,  sometimes  on  both  sides  of  the 
brain.  The  symptoms  are  such  as  might  be  expected 
from  the  irritation  and  compression  of  the  cortex  by 
the  clot — convulsions  (general  or  unilateral),  rigidity, 
opisthotonos  and  hemiplegia,  sometimes  diplegia.  The 
diagnosis  presents  no  difficulties  if  the  occurrence  of 
the  condition  is  remembered,  its  relation  to  injury 
during  labor  (difficult  or  protracted)  being  obtrusively 
clear. 

The  recognition  of  the  second  form  of  meningeal 
hemorrhage — extra  -  dural  hemorrhage ' —  though  often 
easy,  may  be  exceedingly  difficult.  There  is  in  this 
condition  an  extravasation  of  blood  between  the  dura 
and  the  skull  from  the  middle  meningeal  artery..  It 
occurs  usually  on  one  side  of  the  head,  but  sometimes 
the  hemorrhage  occurs  on  both  sides.  Almost  always 
the  injury  which  causes  extra-dural  hemorrhage  gives 
rise  to  fracture  of  the  skull,  and  generally  this  is 
extensive  and  grave  in  character  (vault  and  base). 
The  condition  always  depends  on  direct  injury  to 
the  head,  usually  severe,  but  sometimes,  it  is  important 
to  note,  apparently  trivial  in  character.  Very  often  the 
injury  is  from  a  fall  of  a  serious  character. 

'  This  condition  is  of  frequent  occurrence,  and  is  of  great  import- 
ance, both  medically  and  surgically.  It  is  especially  important  that 
it  should  not  be  confounded  with  hemorrhage  into  the  brain.  In 
many  fatal  cases  of  fracture  of  the  base,  death  depends  on  extra- 
dural hemorrhage — a  condition  which  can  sometimes  be  successfully 
relieved  by  surgical  means. 


THE   DIAGNOSIS    OF   CLINICAL   TYPES.  38 1 

The  chief  clinical  characters  of  extra-dural  hemor- 
rhage are  as  follows  : 

A.  There  is  a  period  of  consciousness  (lucid  interval)^ 
between  the  time  of  injury  and  the  appearance  of  symp- 
toms of  brain  compression.  This  interval  may  be  of 
only  a  few  minutes'  duration,  or  it  may  last  several 
hours  ;  generally  the  interval  is  short  but  well  marked. 
Such  an  interval  is  present  in  considerably  more  than 
half  the  cases  of  extra-dural  hemorrhage,  and  its  pres- 
ence is  therefore  highly  suggestive  of  the  condition.  Its 
absence,  on  the  other  hand,  does  not  in  itself  render  the 
condition  improbable. 

B.  The  lucid  interval  is  followed  by  pressure  symptoms 
of  rapid  or  gradual  onset.  Sometimes  these  symptoms 
supervene  directly  on  the  injury.      They  are  as  follows  : 

a.  Hemiplegia,  partial  or  complete,  preceded  or  ac- 
companied by  convulsions,  usually  unilateral,  but  some- 
times general.  The  hemiplegic  limbs  may  be  rigid  or 
flaccid.  The  knee-jerk  is  usually  but  not  always  lost  on 
the  hemiplegic  side.  Hemiplegia  is  a  very  frequent  and 
characteristic  symptom,  and  in  its  total  absence  the 
diagnosis  of  extra-dural  hemorrhage  cannot  be  made 
with  any  degree  of  certainty. 

b.  Dilatation  and  loss  of  reaction  in  the  pupil  on  the 
side  opposite  the  hemiplegia,  /.  e.,  on  the  side  of  the 
lesion.  This  symptom  is  thought  to  depend  on  pressure 
on  the  third  nerve  at  the  base.  It  is  present  in  a  con- 
siderable proportion  of  all  the  cases  of  extra-dural 
hemorrhage  and  is  a  highly  characteristic  symptom.. 

c.  Stupor  gradually  deepening  into  coma. 

The  diagnostic  value  of  these  symptoms  is  greatly  in- 
creased by  their  association  with  evidences  of  fracture 

^  In  rare  cases  of  extra-dural  hemorrhage  the  lucid  interval  lasts 
several  days. 


382         DISEASES   OF   THE  NERVOUS   SYSTEM. 

of  the  base  of  the  skull,  especially  bleeding  from  the 
ear,  escape  of  the  cerebro-spinal  fluid  and  tumefaction 
about  the  mastoid  process.  Other  less  characteristic  but 
important  symptoms  of  different  frequency  are  repeated 
vomiting,  a  slow  and  hard  pulse,  embarrassed  and  slow 
respiration,  aphasia,  hemianaesthesia  (partial),  loss  of 
sphincteric  control,  contraction  of  the  pupils  and  mod- 
erate fever. 

The  gradual  development  of  anaesthesia  points  to  a 
backward  extension  of  the  hemorrhage  ;  ophthalmoplegia 
to  extension  towards  the  base,  and  aphasia  to  extension 
anteriorly. 

The  distinction  of  extra-dural  hemorrhage  from  medi- 
cal conditions  causing  rapid  or  sudden  loss  of  conscious- 
ness and  focal  symptoms  (hemorrhage,  acute  softening) 
is  usually  not  difficult,  but  in  the  absence  of  any  history 
of  injury,  or  of  evidence  of  fracture  of  the  skull,  the 
diagnosis  may  be  extremely  difficult  or  impossible. 
Other  conditions,  which  are  liable  to  be  confounded 
with  extra-dural  hemorrhage  are:  (i)  laceration  of  the 
brain  *  :  (2)  laceration  of  the  lateral  or  superior  longi- 
tudinal sinus,  with  extravasation  into  the  arachnoid 
cavity,  or  between  the  base  and  dura  ;  and  (3)  hem- 
orrhage into  the  arachnoid  cavity,  not  from  a  sinus. 
All  of  these  conditions  depend  on  injury,  and  any  or  all 
of  them  may  be  associated  with  extra-dural  hemorrhage. 
No  positive  data  can  be  given  for  the  distinction  of  extra- 
dural hemorrhage  and  laceration  of  the  brain,  but  the 
following  facts  may  aid  in  the  diagnosis  :  (a)  In  extra- 
dural hemorrhage  any  wound  or  bruise  is  over  the  posi- 
tion of  the  middle  meningeal  artery  ;  in  laceration  of  the 
brain  it  is  often  on  the  side  opposite  the  lesion.     {^)  In 

'  Generally  the  temporo-sphenoidal,  or  frontal  lobes,  often  on  the 
side  opposite  the  injury. 


THE   DIAGNOSIS    OF   CLINICAL  TYPES.  383 

extra-dural  hemorrhage  there  is  usually  an  interval  of 
lucidity,  and  the  injury  causing  the  condition  may  be 
slight  ;  in  laceration  of  the  brain  there  is  no  interval 
of  lucidity,  and  the  injury  is  always  severe,  (<:)  Severe 
and  persistent  convulsions  on  one  side  of  the  body 
suggest  laceration  of  the  brain,  especially  if  this  con- 
dition be  unassociated  with  hemiplegia.  In  cases  of 
hemorrhage  from  a  sinus  the  position  of  the  wound  is 
a  sufficient  indication  of  the  nature  of  the  condition. 
It  is  practically  impossible  to  make  a  diagnosis  be- 
tween extra-dural  hemorrhage  and  hemorrhage  into 
the  arachnoid.  The  former  is  much  the  more  frequent 
and  important  condition,  and  fortunately  the  treat- 
ment for  it — trephining — is  also  the  proper  treatment 
for  the  latter  condition.  Which  condition  we  have 
to  deal  with  is  perfectly  evident  when  the  button  of 
bone  is  removed  from  the  temporal  region.  In  the 
case  of  extra-dural  hemorrhage  the  clot  lies  next  the 
bone  ;  in  the  case  of  arachnoid  hemorrhage,  if  this  is 
considerable  and  has  caused  symptoms  closely  resemb- 
ling a  typical  extra- dural  hemorrhage,  the  dura  will 
probably  be  found  to  bulge  from  the  pressure  of  the 
clot  beneath  it. 

In  some  cases  of  extensive  Subarachnoid  Hemorrhage^ 
the  symptoms   are   highly  equivocal.     There  may  be  no 

^  Sub-pial  hemorrhage  often  occurs  in  association  with  subdural  or 
subarachnoid  hemorrhage.  Its  symptoms,  if  there  are  any,  are  then 
usually  lost  in  the  more  obtrusive  symptoms  of  the  condition  with 
which  the  sub-pial  hemorrhage  is  associated.  But  sub-pial  hemorrhage 
may  occur  unassociated  with  hemorrhage  elsewhere.  It  depends  in 
such  cases  on  injury  to  the  head  which  causes  severe  concussion  but 
no  fracture.  The  hemorrhage  is  usually  single,  is  located  over  the 
convexity  (especially  of  the  frontal  or  parietal  region),  and  varies  in  size 
from  half  an  inch  to  two  inches  in  diameter.  The  layer  of  extravasated 
blood  is  usually  thin.     If  located  over  the  motor  area  the  hemorrhage 


384         DISEASES   OF   THE   NERVOUS   SYSTEM. 

symptoms  for  four  or  five  days  after  the  injury  except 
slight  headache.  Then  there  may  be  repeated  general 
convulsions  during  several  days,  with  fever  (ioi°-io3^), 
delirium  and  somnolence.  These  symptoms  may  pass 
away  entirely  for  several  days,  and  the  patient  may  ap- 
pear about  to  recover,  when  stupor  reappears,  deepens 
into  coma,  the  temperature  rises  and  the  case  terminates 
in  death.  The  presence  of  convulsions,  headache,  fever 
and  delirium  in  such  a  case  may  lead  to  a  suspicion  of 
meningitis,  but  the  only  form  of  meningitis  that  is  likely 
to  follow  immediately  on  a  severe  injury  to  the  head  is 
suppurative  in  character  and  is  distinguished  by  higher 
fever  and  a  more  rapid  and  progressive  course.  It  is 
important  to  note  the  fact  that  a  slowly  developing  sub- 
arachnoid hemorrhage  (with  a  long  lucid  interval)  may 
cause  no  hemiplegia,  although  the  motor  area  of  the 
brain  is  much  compressed. 

Sinus-Thrombosis. — The  principal  facts  relating 
to  the  pathology  of  sinus-thrombosis  have  been  already 
considered  (p.  267).  Clinically  it  is  necessary  to  keep 
distinct  the  two  forms  of  sinus-thrombosis — primary  or 
marantic  thrombosis  and  secondary  thrombosis. 

a.  Primary  or  Marantic  Thrombosis. — The  symptoms 
that  indicate  this  condition  are  :  (i)  stupor  gradually 
deepening  into  coma,  (2)  general  convulsions  frequently 
repeated  with  or  without  focal  paralysis,  associated  with 
(3)  an  exhausting  disease — as  phthisis  or  cancer  in  its 
last  stages,  long-continued  suppuration,  acute  specific 
disease  or,  most  frequently  of  all,  prolonged  diarrhoea 

may  cause  repeated  convulsions  and  slight  hemiplegic  weakness.  A 
hemorrhage  not  over  the  motor  region  may  cause  no  symptom  except 
stupor,  but  on  the  other  hand  may  cause  repeated  general  convulsions. 
It  may  be  difficult  to  distinguish  between  the  effects  of  the  hemorrhage 
and  those  of  concussion. 


THE   DIAGNOSIS    OF   CLINICAL   TYPES.  385 

during  infancy,  and  (4),  in  some  instances,  distension  of 
external  veins  connected  with  the  sinus  thrombosed. 

In  young  children  (especially  infants),  in  whom  a  very 
large  percentage  of  the  cases  of  marantic  sinus-throm- 
bosis occur,  the  general  cerebral  symptoms  that  result 
from  the  thrombosis  are  often  obscured  by  the  general 
cerebral  symptoms  that  accompany  an  exhausting  diar- 
rhoea, for  stupor,  coma  and  general  convulsions  may 
result  from  the  cerebral  anaemia  which  an  exhausting 
diarrhoea  frequently  induces.  The  diagnosis  of  sinus- 
thrombosis  should  be  suspected  in  young  children  only 
when  there  are  present,  in  addition  to  the  general  cerebral 
symptoms,  symptoms  of  a  focal  character  (local  paraly- 
sis, local  convulsions,  local  rigidity)  or  external  tume- 
faction '  developing  after  the  other  symptoms.  The 
diagnosis  is  to  be  considered  certain  only  in  the  rare 
cases  in  which  the  latter  is  present. 

In  adults  in  whom  there  is  a  cause  for  thrombosis 
(exhausting  disease  —  phthisis,  cancer,  in  terminal 
stage),  marantic  sinus-thrombosis  may  be  suspected. if 
there  are  the  acute  cerebral  symptoms  already  men- 
tioned, provided  there  can  be  excluded  all  causes  of 
arterial  thrombosis  (especially  atheroma,  heart  disease, 
degenerative  time  of  life).  But  here,  as  in  children,  a 
positive  diagnosis  can  be  made  only  in  the  presence  of 
external  distension  of  veins  or  oedema.  It  is  important 
to  note  that  in  persons  over  fifty  the  cerebral  symptoms 
referred  to  are  far  more  apt  to  be  due  to  arterial  throm- 
bosis than  to  sinus-thrombosis. 

^  The  positions  in  which  the  external  distension  of  veins  or  oedema 
occurs  are  :  oedema  and  distension  of  the  veins  on  the  forehead  and 
sides  of  the  head  in  thrombosis  of  the  superior  longitudinal  ;  oedema 
of  the  eyelids  and  temples  in  thrombosis  of  the  cavernous  sinus  ; 
oedema  over  the  mastoid  process  in  thrombosis  of  the  lateral  sinus. 


386         DISEASES   OF   THE   NERVOUS   SYSTEM. 

b.  Secondary  Thrombosis. — There  is  nothing  character- 
istic about  the  symptoms  of  secondary  sinus-thrombosis. 
The  sinus-thrombosis  results  in  most  cases  from  caries 
of  bone,  especially  from  disease  of  the  internal  ear, 
more  rarely  from  meningitis  (especially  tubercular)  and 
suppuration  external  to  the  skull,  and  such  symptoms  as 
are  due  to  the  thrombosis  are  obscured  by  the  more 
obtrusive  evidences  of  the  primary  trouble.  Speaking 
generally,  the  symptoms  that  attend  secondary  sinus- 
thrombosis  closely  resemble  those  of  meningitis  running 
an  acute  or  subacute  course,  and  they  are,  indeed,  usually 
due  to  meningitis.  In  many  cases  the  breaking  down  of 
the  clot,  which  is  septic,  leads  to  symptoms  of  septicae- 
mia. The  conditions,  therefore,  that  suggest  secondary 
sinus-thrombosis  are  :  (i)  the  presence  of  a  cause  of 
secondary  thrombosis  ;  (2)  symptoms  resembling  acute 
or  subacute  meningitis,  associated  with  or  succeeded 
t>y  (3)  symptoms  of  septicaemia.  But  it  is  only  when 
these  symptoms  are  associated  with  external  oedema 
or  venous  distension  that  a  diagnosis  of  secondary 
sinus-thrombosis  can  be  made  with  a  high  degree  of 
probability. 

Infantile  Cerebral  Paralysis. — The  paralyses  of 
cerebral  origin  that  are  frequently  observed  during  in- 
fancy and  childhood  are  not  all  dependent  upon  one  path- 
ological state,  but  may  probably  result  from  any  one  of 
several  distinct  conditions — from  hemorrhage,  arterial  or 
venous  thrombosis,  embolism,  etc.  Notwithstanding  these 
different  modes  of  origin  of  the  infantile  cerebral  paraly- 
ses, their  symptoms  resemble  one  another  so  closely,  what- 
ever may  be  their  origin,  and  their  pathology  is  in  some 
instances  so  obscure,  that  it  is  not  at  present  feasible  or 
desirable  to  classify  them  according  to  the  nature  of  the 
lesions  to  which  they  are  due.     It  is  preferable  to  group 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.  387 

them  all  under  the  clinical  designation  above  adopted — 
infantile  cerebral  paralysis. 

The  clinical  characters  of  infantile  cerebral  paralyses, 
though  differing  widely  in  some  cases,  have  enough 
points  of  resemblance  to  constitute  a  very  distinct  clini- 
cal type.     These  characters  are  as  follows  : 

1.  Motor  paralysis,  usually  hemiplegic  in  form,  occa- 
sionally diplegic  and  rarely  monoplegic.  The  paralysis, 
whatever  may  be  its  form,  has  the  following  features: 

a.  There  is  marked  rigidity  in  the  muscles  paralyzed, 
and  in  most  cases  contractures,  which  may  be  extreme. 

b.  The  knee-jerks  and  reflexes  generally  are  much  ex- 
aggerated. Usually  this  increase  of  reflex  is  most  marked 
on  the  side  paralyzed  if  the  case  be  one  of  diplegia. 

c.  The  paralysis  is  frequently  followed  after  a  time  by 
athetoid,  associated,  choreiform  or  other  movements. 

d.  The  muscles  paralyzed  do  not  present  the  RD, 
and  electrical  changes,  when  present,  are  quantitative  or 
slight  in  degree, 

e.  The  paralysis  is  usually  partial.  If  considerable  at 
first  it  rapidly  lessens.  In  hemiplegic  cases  the  face 
often  escapes  entirely.  The  leg  recovers  more  rapidly 
and  perfectly  than  is  the  case  when  hemiplegia  occurs 
in  the  adult,  and  the  ultimate  paralysis  may  be  chiefly 
in  the  arm. 

/.   There  are  no  disturbances  of  sensibility. 

2.  In  the  cases  of  infantile  cerebral  paralysis  that  de- 
velop in  children  who  have  acquired  language,  transient 
motor  aphasia  is  often  developed.  In  cases  of  hemiplegia 
in  children,  aphasia  is  almost  as  common  when  the  lesion 
is  on  the  right  side  of  the  brain  as  when  it  is  on  the  left 
side. 

3.  In  nearly  all  cases  of  infantile  cerebral  paralysis  there 
is    arrest  or   retardation  of    development    in  the    limbs 


388         DISEASES   OF   THE   NERVOUS   SYSTEM. 

paralyzed.  The  paralyzed  extremities  become  shorter 
and  smaller  than  those  not  paralyzed.  The  arrest  may  be 
noticeable  in  the  shape  of  the  cranium,  and  in  a  diminu- 
tion in  most  of  the  cranial  diameters.  There  are  well- 
marked  vaso-motor  changes  in  the  paralyzed  extremities, 
and  atrophy  of  the  muscles,  slight  or  considerable  in 
degree,  is  usually  present.^ 

4.  Nearly  all  cases  of  infantile  cerebral  paralysis  are  ac- 
companied with  some  degree  of  mental  impairment.  In 
a  small  proportion  there  is  idiocy  (most  often  in  diplegic 
and  paraplegic  cases),  in  others  there  is  imbecility,  and 
most  frequently  there  is  simple  feeble-mindedness  (most 
common  form  in  hemiplegia). 

5.  Nearly  one  half  the  cases  of  infantile  cerebral  par- 
alysis are  followed  by  epilepsy.  In  most  cases  the  form 
is  that  of  general  epilepsy  (grand  mal),with  a  local  onset, 
but  in  a  considerable  number  the  attacks  are  partial,  in- 
complete, or  Jacksonian  in  type.  The  convulsions  persist 
and  sometimes  survive  all  traces  of  the  original  paralysis. 

For  clinical  purposes  it  is  desirable  to  distinguish 
three  types  of  infantile  cerebral  palsy  :  (I.)  Paralysis  of 
intra-uterine  onset  ;  (II.)  palsy  at  birth  ;  (III.)  the 
acquired  form. 

(/.)  hi  Paralysis  of  hiira-uterine  Onset.  In  paralysis 
of  intra-uterine  onset,  which  is  of  comparatively  rare 
occurrence,  the  morbid  lesion  usually  is  parencephaly 
with  large  areas  of  cortical  destruction,  defective  devel- 
opment of  the  pyramidal  tract,  and  imperfect  develop- 
ment of  those  parts  of  the  brain  subserving  the  higher 
mental  processes. 

1  In  rare  instances  hypertrophy  of  paralyzed  parts  occurs  owing  to 
athetosis  and  other  morbid  movements. 


THE   DIAGNOSIS   OF  CLINICAL  TYPES.  389 

(//.)  The  Congenital  Form  of  Infantile  Cerebral  Palsy 
{Cerebral  Birth-Palsy^  Infantile  Meningeal  Hemorrhage). 
— The    congenital    form    of    infantile    cerebral    palsy 


FIG.    78. 
Cerebral  diplegia  (" crossed-leg  progression"). 

(cerebral  birth-palsy,  infantile  meningeal  hemorrhage). 
This  form  of  infantile  cerebral  palsy  depends  on  menin- 
geal hemorrhage  over  one  or  both  sides  of  the  convexity 


390         DISEASES   OF  THE   NERVOUS   SYSTEM. 

of  the  brain  or  on  its  base,  the  result  of  injury  during 
birth.     This  acute  lesion  is  followed  by  chronic  inflam- 


Fio.  79. 

Infantile  cerebral  hemiplegia. 


mation  of  the  cerebral  cortex  and  its  membranes,  finally 
ending  in  diffuse  or  lobar  sclerosis,  cystic  degeneration. 


THE    DIAGNOSIS   OF   CLINICAL   TYPES.  39I 

and  partial  atrophy  of  the  affected  parts.  In  about  two 
thirds  of  the  cases  the  paralysis  is  of  the  hemiplegic  form ; 
in  one  third  it  is  diplegic.  The  facts  that  indicate  the 
existence  of  the  congenital  form  of  palsy  are: 

(i)  A  history  of  hemiplegia  or  diplegia  only  exception- 
ally without  convulsions  dating  from  birth  or  from  a  few 
days  subsequent  to  birth, — though  the  paralysis  may  not 
have  been  observed  for  some*  time  after  parturition. 
There  is  never  a  history  of  distinct  onset  after  birth. 

(2)  There  is  a  history  of  some  distinct  difficulty  in 
birth,  either  an  unnatural  presentation  or  more  fre- 
quently prolonged  and  difficult  labor  with  head  presenta- 
tion in  primipara.  Comparatively  few  instances  can  be 
attributed  to  forceps  delivery  alone.  Precipitate  de- 
livery produces  compression  of  the  head  similar  to  that 
occurring  in  prolonged  labor. 

The  symptoms  in  these  cases  are  those  already 
enumerated  :  Partial  paralysis,  hemiplegia  or  diplegia 
with  rigidity  and  contractures,  arrested  development, 
increased  reflexes,  post-hemiplegic  movements,  mental 
impairment,  and  frequently  epileptic  seizures.  There  is 
nothing  distinctive  about  these  symptoms  or  their  combi- 
nations, and  the  diagnosis  of  this  form  of  cerebral  palsy 
depends  on  the  etiological  facts  above  stated  and  on  the 
absence  of  a  distinct  onset  of  the  symptoms  after  birth 
The  deep  reflexes  on  the  paralyzed  side,  which  are  all 
abolished  for  a  time  after  the  stroke,  are  regained  in  a 
day  or  two  and  remain  permanently  exaggerated.  The 
skin  reflexes,  on  the  other  hand,  are  always  abolished  on 
the  hemiplegic  side.  Dorsi  flexion  of  the  great  toe 
always  occurs  on  the  paralyzed  side  when  the  sole  of 


392        DISEASES   OF  THE  NERVOUS   SYSTEM. 

the  foot  is  stroked.  The  temperature  of  the  hemiplegic 
parts  is  about  a  degree  less  than  on  the  sound  side. 
More  or  less  marked  aphasia  occurs  in  lesions  of  the  left 
hemisphere  in  right-handed  individuals  and  in  the  right 
hemisphere  in  the  left-handed. 

{III.)  The  Acquired  Form  of  Infantile  Cerebral  Palsy 
(Acute  Cerebral  Infantile  Palsy,  Infantile  Hemiplegia). 
There  is  considerable  difference  of  opinion  as  to  the 
pathological  process  which  underlies  the  acquired  form 
of  infantile  cerebral  palsy  and  it  is  certain  that  this  is 
not  the  same  in  all  cases.  The  following  morbid  pro- 
cesses have  been  found  to  underlie  the  condition  : 
Meningeal  hemorrhage  (most  frequent);  thrombosis  of 
superficial  cortical  veins  from  syphilitic  endarteritis  and 
from  atheroma;  hemorrhage,  especially  into  the  cortex, 
or  pia,  or  subarachnoid  space  ;  cerebral  embolism.  ;  and 
last  but  not  least,  an  inflammatory  process  known  as  pol- 
ioencephalitis, involving  the  motor  cortical  ganglion  cells 
and  supposed  to  be  analogous  to  the  process  in  the  spinal 
cord  known  as  poliomyelitis.  There  are  good  reasons 
to  think  that  each  of  these  processes  may  at  times  be 
effective  in  causing  infantile  hemiplegia,  but  in  the  case 
of  thrombosis  of  cortical  veins  and  particularly  of  polio- 
encephalitis this  supposition  is  as  yet  based  chiefly  on 
theoretical  considerations.  The  terminal  states  of  the 
processes  just  enumerated  are  the  same  as  those  in  the 
congenital  form.  Aside  from  a  slight  temporary  awk- 
wardness in  its  use  the  tongue  itself  is  rarely  paralyzed. 

In  the  acquired  form  of  infantile  cerebral  paralysis 
the  form  of  the  paralysis  is  hemiplegic  in  fully  nine 
tenths  of  all  the  cases  ;  diplegias  and  paraplegias 
are  rare  as  compared  with  their  occurrence  in  the  con- 
genital form. 


THE  DIAGNOSIS   OF   CLINICAL   TYPES.  393 

The  recognition  of  this  form  (acquired)  of  cerebral 
paralysis  depends  on  the  following  facts  : 

1.  The  onset  of  the  paralysis  is  acute  or  sudden,  and 
occurs  during  infancy  or  early  childhood.  In  about  one 
half  the  cases  the  onset  is  attended  with  convulsions, 
usually  one-sided,  sometimes  general.  There  may  or  may 
not  be  loss  of  consciousness  lasting  hours  or  days,  and 
there  may  or  may  not  be  fever  and  vomiting  at  the  onset. 

2.  In  nearly  half  the  cases  the  disease  is  distinctly 
secondary  to  some  other  condition.  In  these  cases  the 
exact  period  of  onset  of  the  paralysis  may  be  obscured 
by  the  symptoms  of  the  primary  disease. 

The  conditions  to  which  the  acquired  form  are  most 
often  secondary  are  as  follows  :  pneumonia/  scarlet 
fever,  measles,  whooping-cough  and  injury  to  the  head, 
but  it  occasionally  follows  almost  every  acute  specific  or 
general  disease. 

The  distinction  between  the  two  above-described 
forms  of  infantile  cerebral  paralysis  is  usually  easy,  and 
may  be  made  from  the  facts  already  given  relating  to 
their  etiology  and  mode  of  development. 

The  diagnosis  between  infantile  cerebral  palsy  and 
other  forms  of  brain  disease  is  also  easy  as  a  rule.  The 
hemiplegia  that  occurs  in  tumor  is  distinguished  from 
that  of  acute  infantile  cerebral  palsies  by  the  gradual 
onset  and  progressive  development  of  the  symptoms  of 
the  former  as  distinguished  from  the  acute  onset  and 
stationary  or  retrogressive  character  of  the  symptoms  in 
the  latter. 

Typical  cases  of  infantile  cerebral  paralysis  cannot  be 
confounded  with  typical  cases  of  poliomyelitis — infan- 
tile spinal  paralysis — but  both  are  large  groups,    the 

^  Very  extensive  subarachnoid  hemorrhage  is  sometimes  seen  in  the 
cases  that  develop  during  pneumonia.         * 


394        DISEASES   OF  THE   NERVOUS   SYSTEM. 

variations  within  which  are  such  that  cases  are  met  with 
in  each  that  bear  a  considerable  though  superficial  re- 
semblance to  one  another.  A  case  of  infantile  cerebral 
paralysis  in  which  there  is  considerable  paralysis  and 
atrophy  in  one  arm  (the  leg  having  recovered  partially 
or  entirely),  may  closely  resemble  a  case  of  poliomyelitis 
involving  one  arm,  and  the  resemblance  may  be  height- 
ened by  the  history,  in  both  cases,  of  an  acute  onset  with 
fever  and  convulsions.  In  such  an  instance  the  diagnosis 
would  depend  (chiefly)  on  the  electrical  reactions,  which 
would  be  normal,  or  nearly  so,  in  the  cerebral  case,  but 
would  present  some  form  of  RD  in  the  spinal  case. 

In  the  so-called  paraplegia  form  of  infantile  cerebral 
paralysis  the  palsy  may  possibly  be  confounded  with 
that  from  disease  of  the  spinal  cord.  Close  examination, 
however,  shows,  that  there  is  usually  some  motor  de- 
rangement in  the  upper  extremites  in  the  former  cases. 
It  is  important  also  to  note  that  the  chronic  spastic 
paraplegia  that  results  from  spinal-cord  disease  is  ex- 
ceedingly rare  in  young  children.  If  vertebral  caries  be 
excluded,  such  paraplegia  is  almost  invariably  due  to  a 
cerebral  lesion.     (See  Primary  Spastic  Paraplegia.) 

Abscess  of  the  Brain. — The  symptoms  of  abscess 
of  the  brain  are  exceedingly  variable  and  often  equiv- 
ocal. They  consist,  first,  of  diffuse  symptoms,  which  are 
much  like  those  of  tumor  (see  p.  375) — headache,  vomit- 
ing, optic  neuritis  and  mental  apathy  ;  and,  secondly, 
oi  focal  symptoms,  which  depend  entirely  on  the  situation 
of  the  abscess  and  are  even  more  variable  than  the  dif- 
fuse symptoms.  In  some  cases  the  focal  symptoms  are 
entirely  wanting.  In  many  instances  there  are  in 
addition  to  the  diffuse  and  focal  symptoms  the  general 
symptoms  due  to  suppuration — fever  and  repeated  rigors. 
In  about  three  fourth^  of  all  the  cases  there  is  present  a 


THE   DIAGNOSIS    OF   CLINICAL   TYPES.  395 

distinct  and  recognizable  cause  of  cerebral  abscess,  such 
as  trauma,  caries  of  cranial  bones,  chronic  ear  disease, 
or  suppuration  elsewhere,  as  in  the  lung. 

Of  the  focal  symptoms,  hemiplegia^  often  incomplete,  is 
the  most  constant,  occurring  as  it  does  in  about  half  of 
all  cases  of  cerebral  abscess  Local  convulsions  are  less 
common.  They  are  usually  associated  with  hemiplegia, 
and  both  symptoms  depend  on  the  location  of  the  lesion 
near  or  in  the  motor  path.  When  there  is  a  considerable 
degree  of  paralysis  of  one  side  there  is  almost  always  a 
great  exaggeration  of  the  knee-jerk  on  this  side  usually 
with  very  pronounced  ankle  clonus^  and  Babinski's  sign. 

The  course  of  abscess  of  the  brain  is  exceedingly  varia- 
ble and  necessitates  the  recognition  of  two  groups  of 
cases :  first,  cases  which  run  an  acute  course,  and, 
secondly,  cases  which  run  a  chronic  course. 

1.  The  acute  cases  are  those  that  commence  with  well 
marked  cerebral  symptoms — headache,  vomiting,  etc., — 
which  progress  rapidly,  and  without  distinct  diminution, 
into  a  stage  characterized  by  severe  general  cerebral 
symptoms — headache,  vomiting,  optic  neuritis,  general 
convulsions,  and  mental  apathy,  delirium  and  coma  ;  per- 
haps also  by  focal  symptoms — hemiplegia  and  local  con- 
vulsions. This  is  the  terminal  stage.  The  entire  course 
of  the  disease  varies  in  these  acute  cases  from  a  week  to 
a  month. 

2.  The  chronic  cases  are  those  in  which  there  is  a 
long  period  of  latency  between  the  initial  and  terminal 

^  Ankle  clonus,  we  believe,  is  a  very  regular~symptom  in  cases  of 
cerebral  abscess  involving  the  motor  path,  and  is  often  seen  in  cases 
of  abscess  of  the  frontal  lobe  reaching  back  and  slightly  encroaching 
upon  the  motor  path.  Violent  clonus  may  be  obtainable  where  there 
is  very  slight  motor  paralysis. 


396        DISEASES   OF   THE   NERVOUS  SYSTEM. 

cerebral  symptoms,  the  former  being  often  so  slight  as 
to  be  entirely  overlooked. 

This  period  of  latency  may  last  weeks,  months,  or 
years,  and  may  be  complete  or  incomplete.  If  incom- 
plete, there  may  be  present  some  equivocal  cerebral 
symptoms,  as  headache,  occasional  vomiting,  convulsions, 
slight  mental  failure,  apathy,  etc.  Then,  after  a  variable 
time,  all  these  symptoms  increase,  and  pass,  gradually  or 
rapidly,  into  a  terminal  stage  like  that  above  described, 
characterized  by  headache,  convulsions,  optic  neuritis, 
delirium  and  stupor  deepening  into  coma.  If  the 
latency  is  complete  there  are  no  recognizable  evidences 
of  brain  disease  until  the  terminal  stage  of  grave  cerebral 
symptoms  is  suddenly  or  rapidly  reached. 

In  those  cases  of  abscess  in  which  there  are  well- 
marked  general  and  local  cerebral  symptoms  and  symp- 
toms indicative  of  a  suppurative  process — fever  and 
repeated  rigors,  in  the  presence  of  a  cause  {vide  ante) 
that  is  adequate  to  account  for  a  cerebral  abscess — the 
diagnosis  is  not  difficult.  In  those  cases,  however,  in 
which  the  period  of  latency  is  complete,  or  nearly  so, 
and  the  terminal  symptoms  come  on  suddenly  or  rapidly, 
a  diagnosis  of  apoplexy  from  cerebral  hemorrhage  or 
acute  cerebral  softening  may  be  erroneously  made.  Such 
an  error  may  be  avoided  if  a  recognizable  cause  for 
abscess  exists  and  leads  to  a  suspicion  of  abscess. 
Hemorrhage  and  softening  could  be  positively  excluded 
if  examination  revealed  the  existence  of  optic  neuritis 
in  the  absence  of  chronic  diffuse  nephritis. 

The  two  diseases  with  which  abscess  is  most  often  con- 
founded are  tumor  and  meningitis.  The  points  of  dis- 
tinction from  the  former  are  given  on  page  379.  The 
diagnosis  between  abscess  and  meningitis  has  been  given 
elsewhere  (see  p.  343). 


THE   DIAGNOSIS    OF   CLINICAL   TYPES.  397 

Intracranial  Tumor. — The  symptoms  that  point 
to  the  existence  of  a  tumor  within  the  cranial  cavity  are 
of  two  kinds — diffuse  or  general  and  focal.  The  most 
significant  and  frequent  diffuse  symptoms  are  :  (i)  head- 
ache— severe  and  persistent  ;  (2)  vomiting — especially 
without  gastric  cause  and  (3)  double  optic  neuritis. 
Other  diffuse  symptoms  of  importance  are  ;  (i)  general 
convulsions  ;  (2)  attacks  of  petit  mal ;  (3)  giddiness  ; 
(4)  slowness  of  speech  ;  (5)  simple  mental  failure  ;  and 
as  terminal  symptoms,  (6^)  stupor  and  coma.  The 
focal  symptoms,  unlike  the  diffuse  symptoms,  depend  on 
the  situation  of  the  tumor  and  afford  an  indication  of 
its  position.  Some  of  the  focal  symptoms  are  irritative 
in  character,  others  destructive.  The  symptoms  and 
their  combinations  that  depend  on  the  position  of  the 
tumor  within  the  cranium  maybe  inferred  from  the  facts 
of  localization  already  presented  (see  Chap.  III).  The 
focal  symptoms  of  tumor  that  are  of  most  frequent 
occurrence  are  :  (i)  motor  paralysis,  usually  of  local 
commencement  (monoplegia)  with  subsequent  extension 
(hemiplegia  or  partial  hemiplegia)  ;  (2)  local  spasm — 
corresponding  to  the  seat  of  the  motor  paralysis  ;  (3) 
aphasia — usually  motor,  sometimes  sensory  ;  (4)  dis- 
turbances of  sensibility  ;  (5)  paralyses  of  cranial  nerves. 

An  exceedingly  important  general  characteristic  of  all 
these  symptoms  of  tumor  is  that  they  are  oi  gradual  onset 
and  run  a  gradually  progressive  course.  The  gradual 
onset  is  as  distinctive  of  tumor  as  is  the  sudden  onset  of 
vascular  disease — cerebral  hemorrhage  and  acute  cere- 
bral softening.  It  is  important  to  note,  however,  (i) 
that  the  course  of  the  tumor  is  not  usually  uniformly 
progressive — periods  of  intermission  often  alternating 
with  periods  of  progress  ;  and  (2)  that  sometimes  symp- 
toms increase  rapidly  in  intensity  by  causing  inflamma- 


398         DISEASES   OF   THE   NERVOUS   SYSTEM. 

tion  in  neighboring  structures  ;  and  (3)  that  some  forms 
of  tumor  (glioma)  may  cause  symptoms  of  sudden  onset 
from  rupture  of  vessels  within  their  substance. 

When  the  diagnosis  of  tumor  has  been  made  and  the 
position  of  the  growth  determined  by  the  rules  of  local- 
ization already  given  {vide  ante),  it  remains  to  fix  upon  the 
nature  of  the  growth.  Sometimes  this  can  be  done  with  a 
high  degree  of  probability,  or  even  with  certainty  ;  more 
often  the  diagnosis  of  the  nature  of  the  tumor  can  be 
narrowed  down  to  one  of  two  possibilities  ;  and  more  often 
still  the  data  afford  a  basis  for  nothing  more  than  a  guess. 

Syphilomata,  tubercular  growths,  sarcomata  (including 
gliomata),  and  carcinomata  probably  make  up  at  least 
nine  tenths  of  all  intra-cranial  growths.  In  other  forms 
of  tumor  it  is  impossible  in  a  very  large  majority  of 
cases  to  make  a  pathological  diagnosis.  The  diagnostic 
effort  is  therefore  practically  limited  to  the  cases  included 
in  the  first  group. 

The  indications  that  suggest  that  the  tumor  is  a 
syphilitic  growth  are  as  follows  : 

1.  A  distinct  history  or  symptoms  of  constitutional 
syphilis.' 

2.  Symptoms  indicating  that  the  tumor  is  in  the  cor- 
tex of  the  brain  (see  Localization),  and  is  producing 
irritative  rather  than  destructive  phenomena. 

3.  Evidences  of  rapid  growth  at  the  onset,  followed 
by  a  period  of  slow  growth  or  a  stationary  condition. 

4.  Retrogression  and  gradual  arrest  of  the  symptoms 
of  a  tumor  under  antisyphilitic  treatment  (iodide  and 
mercury). 

'  A  history  of  a  chancre  without  secondaries  has  a  similar  significance. 
A  syphiloma  cannot,  of  course,  be  excluded,  unless  the  possibility  of 
syphilitic  infection  can  be  also  excluded.  It  must  be  remembered 
that  a  growth  of  another  nature  may  coexist  with  syphilis. 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.  399 

5.  The  development  of  the  tumor  during  early  or 
middle  adult  life  (twenty  to  forty-five  years).  This  is, 
of  course,  of  little  value,  as  most  forms  of  tumor  are  most 
common  at  this  period. 

The  indications  that  suggest  a  tubercular  growth  are  : 

1.  The  presence  of  tubercular  disease  in  some  other 
organ  than  the  brain,  or  a  family  history  of  tubercular 
disease, 

2.  A  rapid  development  of  the  symptoms,  which  after 
a  time  become  stationary. 

3.  Symptoms  indicating  that  the  tumor  is  in  the  cere- 
bellum or  in  the  pons. 

4.  The  development  of  the  symptoms  before  the 
twentieth,  and  especially  before  the  tenth  year.  This 
indication  refers  also  to  glioma. 

5.  A  history  of  injury  to  the  head. 

6.  Improvement  under  tonic  treatment. 

The  indications  that  suggest  the  existence  of  a  sarcoma 
are  :  (i)  the  presence  of  a  sarcomatous  tumor  else- 
where (this  makes  the  probability  very  high)  ;  evidence 
that  the  tumor  is  not  in  the  brain  substance  itself,  as 
when  it  is   in  the  bones  (rarely  available). 

The  following  indications  suggest  a  glioma  : 

1.  The  occurrence  of  sudden  loss  of  consciousness, 
with  exacerbation  of  all  symptoms,  in  the  course  of  a 
tumor.     This  is  practically  confined  to  glioma. 

2.  The  situation  of  the  tumor  in  the  cortex,  with  pre- 
dominance of  irritative  symptoms.  This  character  is 
shared  with  syphiloma. 

3.  The  absence  of  all  evidence  of  tubercular  and 
syphilitic  disease  and  of  sarcoma  or  carcinoma  in  other 
parts  of  the  body. 

4.  The  age  of  the  patient  is  under  fifty.  If  over  fifty, 
glioma  is  improbable. 


400        DISEASES   OF  THE   NERVOUS   SYSTEM. 

A  carcinoma  is  suggested  by  : 

1.  The  presence  of  carcinoma  elsewhere.  This  makes 
the  diagnosis  highly  probable. 

2.  By  the  patient's  being  over  fifty  years  of  age. 
Tumor  of  the  brain  may  be  confounded  with  other 

organic  diseases  of  the  brain,  with  functional  diseases 
of  the  nervous  system  and  with  diseases  outside  the 
nervous  system. 

Diagnosis  from  Other  Organic  Diseases  of  the  Brain. 
— All  organic  diseases  of  the  brain  may  be  roughly  but 
conveniently  divided  into  two  great  groups  ; — that  in 
which  the  symptoms  are  of  sudden  onset,  and  that  in 
which  the  onset  of  the  symptoms  is  more  or  less  gradual. 
The  first  group  comprises  a  large  and  very  important 
part  of  all  organic  brain  diseases — cerebral  hemorrhage, 
and  the  various  forms  {vide  ante)  of  acute  cerebral  soften- 
ing. Cerebral  tumor  is  distinguished  from  the  members 
of  this  group  of  vascular  lesions,  by  the  simple  but  im- 
portant fact  that  its  symptoms  are  never  of  sudden  onset 
and  never  reach  a  considerable  degree  of  development  in 
the  course  of  a  few  hours.  In  rare  cases  of  tumor 
(especially  cases  of  glioma),  sudden  symptoms  sug- 
gesting a  vascular  lesion  occur,  but  these  symptoms  (which 
are,  indeed,  due  to  hemorrhage  from  rupture  of  vessels 
in  the  tumor)  always  follow  symptoms  of  more  gradual 
onset.  It  is  therefore  necessary  to  consider  only  the  dis- 
tinction of  tumor  from  the  diseases  that  comprise  the 
second  group  above  mentioned — in  which  the  develop- 
ment of  the  symptoms  is  more  or  less  gradual.  This 
group  includes  the  following  conditions :  meningitis, 
acute  and  chronic,  abscess,  aneurism,  general  paralysis, 
insular  sclerosis  and  bulbar  paralysis. 

For  the  diagnosis  between  tumor  and  meningitis,  see 
page  342. 


THE   DIAGNOSIS   OF  CLINICAL  TYPES.         40I 

Diagnosis  behveen  Tumor  and  Abscess. — Cases  of  ab- 
scess occur  that  bear  a  close  resemblance  to  tumor.  The 
diffuse  symptoms,  especially,  are  often  those  of  tumor 
— there  is  headache,  vomiting,  double  optic  neuritis  and 
mental  failure.  If  there  are  well  marked  and  progressive 
focal  symptoms — as  monoplegia,  hemiplegia,  paralysis  of 
cranial  nerves,  etc.,  this  is  in  favor  of  tumor.  The 
absence  of  focal  symptoms  points  to  abscess.  If  there 
is  a  considerable  grade  of  optic  neuritis,  this  is  some- 
what in  favor  of  tumor,  and  if  the  optic  neuritis  is 
intense  (six  dioptrics  or  more),  the  diagnosis  of  tumor  is 
practically  certain.  On  the  other  hand,  a  period  of  con- 
siderable duration  in  which  the  symptoms  are  slight  and 
stationary,  followed  by  a  period  of  rapid  increase  in  the 
severity  of  the  symptoms,  is  in  favor  of  abscess.  The 
occurrence  of  fever  and  rigors,  especially  if  associated 
with  exacerbation  of  the  symptoms,  points  to  abscess. 
If  severe  symptoms  of  rapid  onset  gradually  lessen,  this 
is  in  favor  of  tumor.  The  etiology  may  give  important 
aid  in  the  distinction.  The  absence  of  any  traceable 
cause  for  the  disease  is  distinctly  in  favor  of  tumor  if  the 
symptoms  are  equivocal  If  there  is  ear  disease,  or  dis- 
ease of  the  cranial  bones,  or  a  distant  focus  of  suppura- 
tion, this  makes  abscess  more  than  probable.  If,  how- 
ever, there  has  been  an  injury  to  the  head,  this  gives  no 
help,  for  although  injury  is  more  commonly  a  cause  of 
abscess  than  of  tumor  this  is  compensated  by  the  fact 
that  tumor  is  a  more  common  condition  than  abscess. 

The  diagnosis  between  tumor  and  the  cases  of  hysteria 
that  resemble  it  is  ordinarily  very  simple  ;  yet  such  cases 
are  not  rarely  mistaken  for  tumor,  and  even  more  often 
cases  of  tumor  are  regarded  as  instances  of  hysteria. 
These  errors  would  seldom  or  never  be  made  were  the 
facts  relating  to  the  distinction  of  functional  and  organic 


402         DISEASES   OF   THE   NERVOUS    SYSTEM. 

disease  elsewhere  considered  (see  Chapter  VI.)  borne  in 
mind.  Only  the  main  points  of  distinction  will  be  con- 
sidered here. 

The  cases  of  hysteria  that  are  mistaken  for  tumor  are 
usually  those  in  which  there  are  well  marked  unilateral 
manifestations, — local  paralysis,  monoplegia,  or  hemi- 
plegia, contractures,  spasm,  local  anaesthesia  or  hemian- 
aesthesia.  There  may  be  in  these  cases  a  considerable  de- 
gree of  headache,  there  may  be  repeated  vomiting,  and 
there  may  be  general  convulsions — each  of  which  increases 
the  resemblance  to  tumor.  The  peculiar  distribution  of 
the  hysterical  paralyses  and  anaesthesias,  their  rapid  onset 
after  some  emotional  disturbance,  the  absence  of  local 
convulsions  and  of  unilateral  changes  in  the  reflexes, 
the  absence  of  optic  neuritis  and  the  variations  that  oc- 
cur in  the  hysterical  symptoms  make  the  distinction  easy, 
especially  in  patients  showing  the  mental  characteristics 
of  hysteria.  The  error  of  ascribing  the  symptoms  of 
tumor  to  hysteria  is  generally  made  in  young  women  who 
have  an  inclination  to  emotional  disturbance,  which,  in 
the  presence  of  organic  disease  has  led  to  the  develop- 
ment of  distinct  hysterical  symptoms.  In' other  words, 
in  such  a  case  the  symptoms  of  tumor  are  associated  with 
and  perhaps  somewhat  obscured  by  the  existence  of  true 
manifestations  of  hysteria.  Error  can  always  be  avoided 
by  remembering  that  no  symptom  or  symptoms  should  be 
attributed  to  hysteria  until  the  various  evidences  of  or- 
ganic disease  have  been  eliminated  by  a  careful  search. 
In  tumor  of  the  brain  there  are  always  some  distinct 
indications  of  organic  disease — as  optic  neuritis,  focal 
paralysis,  local  convulsions,  etc.,  which  it  is  inexcusable 
to  overlook. 

Cerebral  tumor  may  be  confounded  with  idiopathic 
epilepsy  in  cases  where  the  tumor  runs  a  slow  course  and 


THE   DIAGNOSIS    OF   CLINICAL   TYPES.  403 

general  convulsions  constitute  a  conspicuous  symptom. 
The  convulsions  of  tumor  usually  have  a  local  com- 
mencement and  this  is  an  important  point  of  difference 
from  those  of  epilepsy,  but  does  not  constitute  an  abso- 
lute criterion,  since  the  local  commencement  may  be 
absent  in  tumor  and  is  in  rare  cases  present  in  epilepsy. 
An  aura,  particularly  a  special  sense  aura,  preceding 
the  attacks  is  rather  in  favor  of  tumor.  But  it  is  rarely 
necessary  to  base  the  distinction  on  these  features  ; 
other  evidences  of  organic  disease  are  usually  present, 
— e.  g.^  there  is  optic  neuritis,  or  there  is  organic  headache, 
or  local  paralysis.  In  the  absence  of  more  unequivocal 
indications,  a  neurotic  heredity,  as  of  epilepsy,  chorea, 
or  hysteria,  may  be  allowed  some  weight  as  increasing 
the  probabilities  of  functional  disease. 

The  error  of  ascribing  a  combination  of  optic  neuritis 
and  headache  in  cases  of  extreme  anaemia,  Bright's  dis- 
ease or  lead  poisoning,  to  an  organic  cause  (and  espe- 
cially to  tumor),  has  already  been  mentioned  (see  optic 
neuritis),  and  does  not  require  further  consideration 
here. 

Intracranial  Aneurism.  —  The  term  intracranial 
aneurism  as  here  employed  relates  only  to  aneurisms  of 
the  main  cerebral  arteries,  and  not  to  the  miliary  aneu- 
risms that  occur  on  their  branches  within  the  brain  sub- 
stance. Miliary  aneurisms  give  rise  to  no  symptoms 
until  rupture  occurs,  and  then  the  symptoms  are  those  of 
cerebral  hemorrhage.  Intracranial  aneurisms,  when  they 
attain  a  considerable  size  and  press  upon  important 
structures,  give  rise  to  symptoms,— differing  in  this  re- 
spect from  miliary  aneurisms.  But  it  is  important  to  note 
that,  in  many  instances,  intracranial  aneurisms,  like  miliary 
aneurisms,  cause  no  symptoms  until  they  rupture. 

The  symptoms  of  aneurism,  when, they  occur,  are  those 


404         DISEASES   OF   THE   NERVOUS   SYSTEM. 

of  a  small  tumor  at  the  base  of  the  brain,  pressing  usually 
either  upon  the  motor  tract  or  upon  the  cranial  nerves,  or 
upon  both.  A  certain  diagnosis  of  the  presence  of  aneu- 
rism can  be  made  only  in  cases  where  there  is  an  aneuris- 
mal  murmur  that  is  distinguishable  on  auscultation  of  the 
skull.  Such  a  murmur  is  heard  only  in  rare  cases  of  intra- 
cranial aneursim,  and  probably  only  in  cases  where  the 
aneurism  is  situated  either  on  the  internal  carotid  or  the 
vertebral  artery.  Hence  a  positive  diagnosis  of  aneurism 
can  be  made  only  in  very  exceptional  instances.  The 
cases  are,  however,  much  more  numerous  where  a^  suspi- 
cion of  aneurism  is  justified,  or  where  even  a  probable 
diagnosis  can  be  made.  The  indications  that  make  the 
diagnosis  of  aneurism  more  or  less  probable  in  the  pres- 
ence of  symptoms  of  a  basal  tumor  are  as  follows  : 

1.  The  history  or  presence  of  a  cause  of  aneurism 
which  is  not  also  a  cause  of  new  growths  within  the 
cranium.  Such  causes  are  (a)  arterial  degeneration  and  (d) 
endocarditis.  Arterial  degeneration,  fibroid  or  atheroma- 
tous, is  sometimes  a  cause  of  aneurism  in  persons  over 
forty.  In  many  cases  of  aneurism  occurring  in  persons 
under  forty  years  of  age  there  are  indications  of  past  or 
present  endocarditis.  The  significance  of  this  circum- 
stance depends  on  the  fact  that  many  cases  of  aneurism 
depend  on  embolism.  Syphilis,  by  causing  endarteritis, 
is  a  cause  of  aneurism,  but  a  history  of  syphilis  has  no 
diagnostic  value,  as  specific  disease  is  more  frequently  a 
cause  of  syphiloma  or  chronic  syphilitic  meningitis  than 
of  aneurism.  A  history  of  injury  (which  is  frequent  in 
aneurism)  is  likewise  of  no  value,  because  injury  is  a 
cause  both  of  aneurism  and  tumor. 

2.  Indications  that  the  tumor  (lesion)  is  in  the  position 
of  a  large  artery.  The  most  common  positions  for  aneu- 
rism are,  first,  on  the  middle  cerebral  artery,  next  on  the 


THE   DIAGNOSIS    OF   CLINICAL   TYPES.         405 

basilar  and  internal  carotid  arteries.  Much  less  often 
aneurisms  are  situated  on  the  anterior  cerebral,  posterior 
communicating,  anterior  communicating,  vertebral,  or 
posterior  cerebral  arteries.  The  focal  pressure  symptoms 
that  result  from  an  aneurism  in  these  different  positions 
may  be  inferred  from  the  relations  of  the  vessels  to  sur- 
rounding parts,  but  the  symptoms  that  result  from  aneu- 
rism on  the  middle  cerebral,  basilar,  and  internal  carotid 
arteries  may  be  briefly  summarized  as  they  comprise 
two-thirds  of  all  cases  of  intracranial  aneurism: 

a.  Middle  Cerebral. — Hemiplegia  and  convulsions  are 
common — paralysis  of  cranial  nerves  rare.  When  on  the 
left  side  there  may  be  motor  aphasia. 

b.  Basilar. — The  symptoms  are  those  due  to  pressure, 
unilateral  or  bilateral,  on  the  pons  and  on  the  cranial 
nerves.  The  nerves  affected  are  generally  several  and  vary 
according  to  the  position  of  the  aneurism  on  the  artery. 
The  5th,  6th,  7th,  8th,  9th,  loth,  and  nth  may  be  affected 
and  usually  in  the  frequency  of  the  order  named,  only 
rarely  the  3d  or  12th.  There  may  be  severe  occipital 
headache.  There  may  be  crossed  paralysis.  There 
are  no  symptoms  in  about  one-third  of  all  cases.  Con- 
vulsions are  uncommon. 

c.  Internal  Carotid, — The  chief  pressure  symptoms  are 
blindness  of  one  eye  from  pressure  on  the  optic  nerve, 
combined  with  paralysis  of  one  or  more  ocular  nerves — 
especially  ptosis — from  pressure  on  the  nerves  in  the 
cavernous  sinus.  Smell  may  be  lost  and  occasionally 
there  may  be  symptoms  of  pressure  on  one  crus. 

In  any  case  where  an  intracranial  aneurism  is  suspected 
the  diagnosis  is  much  strengthened  if  rupture  occurs, 
which  usually  happens  in  one-half  the  cases.  Such  a 
rupture  gives  rise  to  the  symptoms  of  severe  apoplexy. 
If  there  have  been  no   symptoms    to  suggest   aneurism 


406         DISEASES    OF   THE   NERVOUS   SYSTEM. 

before  rupture  occurs,  the  cause  of  the  apoplexy  would 
be  suspected  only  in  case  it  occurred  in  a  person  under 
forty  years  of  age  who  had  suffered  from  endocarditis 
or  syphilis,  or  who  gave  a  history  of  trauma  to  the  head. 

The  chief  conditions  from  which  aneurism  has  to  be  dis- 
tinguished are  intracranial  tumor  and  chronic  syphilitic 
basilar  meningitis.  The  points  on  which  the  distinction 
from  tumor  is  made,  when  this  is  practicable,  have  been 
mentioned  above.  The  question  of  a  diagnosis  from 
chronic  syphilitic  meningitis  arises  in  cases  where  there 
is  pressure  only  upon  cranial  nerves.  The  distinction  is 
frequently  impossible,  especially  if  there  is  a  distinct 
history  of  syphilis.  The  chief  criterion  in  such  instances 
is  that  afforded  by  the  effect  of  antisyphilitic  treatment  : 
in  chronic  meningitis  there  is  regularly  improvement 
under  treatment  ;  in  aneurism  there  is  none.  But  this 
indication,  while  valuable,  is  far  from  absolute. 

Nuclear  Ophthalmoplegia  (Nuclear  Ocular  Paraly- 
sis).— Disease  of  the  nuclei  of  the  motor  nerves  of  the 
eye  (third,  fourth,  and  sixth)  is  often  the  cause  of  paraly- 
sis of  the  ocular  muscles — both  the  external  muscles  of 
the  eyeball  (extrinsic  muscles  of  the  eye)  and  the  mus- 
cles within  the  globe  (internal  or  intrinsic  muscles).  In 
some  cases  the  paralysis  is  the  result  of  involvement  of 
an  isolated  nucleus  ;  in  others,  several  or  all  of  the 
nuclei  are  affected.  Some  of  the  lesions  that  cause 
nuclear  paralysis  are  acute  in  their  development ;  others 
are  chronic.  Thus  it  is  that  the  symptoms  of  nuclear 
ophthalmoplegia  vary  widely  in  different  cases,  according 
to  the  position  and  nature  of  the  morbid  process. 

It  is  desirable  to  distinguish  clinically  two  different 
forms  of  ophthalmoplegia — an  acute  form  and  a  chronic 
form.  Owing  to  its  far  greater  importance  the  chronic 
form  will  be  first  considered. 


THE   DIAGNOSIS   OF    CLINICAL    TYPES.         407 

Chronic  Nuclear  Ophthalmoplegia  (Chronic  Progressive 
Ophthalmoplegia/  Chronic  Nuclear  Paralysis,  Chronic 
Ophthalmoplegia). — The  symptoms  of  chronic  nuclear 
ophthalmoplegia  vary  so  widely  in  different  cases  that  it  is 
difficult  to  say  what  constitutes  the  most  typical  form  of 
the  disease.  The  following  are  the  chief  characteristics 
of  the  disease  : 

I .  The  gradual  and  successive  paralysis  of  many  or  all  of 
the  ocular  muscles. 

At  first  only  a  small  number  of  muscles  (or  one 
only)  is  affected.  One  of  the  first  indications  of  this 
involvement  is  often  double  vision  (usually  transient). 
The  loss  of  power  is  at  first  slight,  but  gradually  increases 
and  extends  to  other  muscles  than  those  first  affected. 
After  the  lapse  of  years  most  of  the  muscles  of  both 
eyes  become  involved,  and  even  all  of  them  may  be  in- 
cluded in  the  paralysis  (total  ophthalmoplegia).  The 
isolated  loss  of  reflex  action  of  the  iris  and  the  isolated 
paralysis  of  the  ciliary  muscle  are  to  be  regarded  as 
varieties  of  chronic  progressive  ophthalmoplegia.  Usu- 
ally the  muscles  are  involved  in  a  random  irregular  man- 
ner without  reference  to  their  function  (this  is  somewhat 
characteristic  of  nuclear  disease),  but  not  rarely  the 
muscles  first  affected  are  associated  in  action  (as  the 
external  rectus  of  one  side  and  the  internal  rectus  of  the 
other,  or  both  internal  recti,  or  the  superior  recti  and 
levators).  Ptosis  is  usually  absent,  and  when  present  is 
rarely  complete.  Nystagmus  and  slight  exophthalmos 
are  occasional  symptoms.  The  process  is  sometimes 
much  more  advanced  in  one  eye  than  in  the  other,  and 
occasionally  the  paralyses  are  all  unilateral.     The  intrin- 

^  Chronic  progressive  ophthalmoplegia  is  so  commonly  caused  by 
nuclear  disease  that  the  term  is  used  synonymously  with  nuclear 
disease. 


408         DISEASES   OF   THE   NERVOUS   SYSTEM. 

sic  muscles  of  the  eye,  though  commonly  affected  in 
some  degree,  may  escape  entirely. 

Most  cases  of  chronic  ophthalmoplegia  are  slowly 
progressive,  though  in  some  cases  there  is  little  prog- 
ress for  many  years.  Occasionally  cases  which  are 
unquestionably  of  nuclear  origin,  after  reaching  an  ad- 
vanced stage  of  paralysis  in  both  eyes,  regain  perfectly 
the  power  of  movement  in  both  eyes.  Such  cases  cannot 
at  present  be  satisfactorily  explained. 

2.  The  association  of  these  ocular  paralyses  with  evi- 
dences of  other  diseases  of  the  nervous  syste?n. 

Sometimes  chronic  ophthalmoplegia  exists  by  itself, 
but  more  often  it  is  associated  with  other  forms  of 
nervous  disease.  Of  these  other  forms  the  most  com- 
mon are  locomotor  ataxia,  general  paralysis  of  the  insane, 
multiple  sclerosis  and  optic-nerve  atrophy.  Psychical 
disturbance  is  a  common  association  ;  sometimes  this  is 
the  precursor  of  the  symptoms  of  general  paralysis.  In 
other  cases  the  mental  disturbance  is  apparently  func- 
tional (hypochondriasis,  hallucinatory  insanity).  The 
relation  of  chronic  ophthalmoplegia  to  the  associated 
condition  varies  in  different  cases.  Either  the  nervous 
disease  or  the  associated  state  may  give  rise  to  the  first 
symptoms,  and  in  some  cases  both  sets  of  symptoms 
appear  and  develop  almost  simultaneously. 

The  lesion  on  which  chronic  nuclear  ophthalmoplegia 
depends  is  a  slow  degenerative  process  in  the  nuclei 
corresponding  to  the  muscles  paralyzed.  In  a  consid- 
erable proportion  of  these  cases  a  syphilitic  history  can 
be  traced,  and  is  probable  in  many  cases  where  it  cannot 
be  traced,  but  there  are  many  cases  in  which  no  cause 
whatever  can  be  found.  Sometimes  ophthalmoplegia  is 
a  congenital  and  perhaps  an  hereditary  condition. 

The  diagnosis  of  chronic  nuclear  ophthalmoplegia  will 


THE   DIAGNOSIS    OF   CLINICAL  TYPES.  409 

be  touched  upon  after  briefly  alluding  to  the  acute  form 
of  the  disease. 

Acute  Nuclear  Ophthalmoplegia. — In  rare  instances  many 
or  all  of  the  ocular  muscles  are  suddenly  or  rapidly  para= 
lyzed  from  disease  of  their  nuclei,  and  this  condition  is 
called  acute  nuclear  ophthalmoplegia.  In  some  cases  the 
condition  has  been  due  to  hemorrhage,  in  others  to  acute 
softening,  in  the  region  of  the  third  nerve  nuclei.  Whether 
it  is  ever  really  due  to  acute  inflammation  of  the  nuclei 
(so-called  acute  polioencephalitis  superior)  is  doubtful. 
Perhaps  some  cases  of  diphtheritic  ocular  paralysis  (in- 
cluding the  common  form  of  paralysis  of  the  ciliary 
muscle-cycloplegia)  are  examples  of  nuclear  disease. 

Having  established  the  existence  of  paralysis  of  ocular 
muscles,  an  effort  must  be  made  to  determine  whether  the 
lesion  is  of  nuclear  origin  or  of  peripheral  origin.  In 
some  cases  a  conclusion  can  be  reached  which  is  almost 
positive  ;  in  other  cases  it  is  impossible  to  reach  a  conclu- 
sion. The  indications  upon  which  the  diagnosis  is  based 
differ  somewhat  in  acute  and  chronic  cases  of  ocular 
paralysis,  and  it  is  convenient  to  consider  them  separately. 

In  cases  of  acute  development  a  nuclear  lesion  is  proba- 
ble if  the  muscles  paralyzed  correspond  to  an  irregular 
involvement  of  the  functions  of  the  nerve  structures,  or 
if  the  muscles  paralyzed  are  very  unequally  involved. 
Thus,  if  several  of  the  muscles  innervated  by  the  third 
nerve  are  paralyzed  without  reference  to  function  (<?.  g.^ 
the  internal  and  inferior  recti),  it  is  highly  improbable 
that  the  lesion  is  peripheral.  Again,  if  all  or  nearly  all 
the  external  muscles  of  the  eyeball  are  involved,  but  some 
(as  the  levator)  are  much  less  paralyzed  than  the  others, 
this  suggests  a  nuclear  lesion.  If  the  intrinsic  muscles  of 
the  eye  escape  entirely,  while  the  external  muscles  are 
extensively  involved,  a  nuclear  lesion  is  almost  certain. 


4IO         DISEASES    OF   THE    NERVOUS   SYSTEM. 

All  these  indications  except  the  last  are  greatly  strength- 
ened in  significance  if  the  palsy  of  the  ocular  muscles  is 
bilateral.  In  acute  or  subacute  palsies  the  associated 
symptoms  may  throw  light  on  the  position  of  the  lesion. 
Thus,  if  the  symptoms  are  such  as  to  suggest  a  quadri- 
geminal  lesion  (see  Localization),  it  is  certain  that  the 
ocular  palsy  is  nuclear.  The  probable  nature  of  the 
lesion  may  aid  in  the  diagnosis.  Vascular  lesions,  for 
example  (hemorrhage,  acute  softening),  can  give  rise  only 
to  nuclear  paralysis,  or  to  fascicular  paralysis,  /.  ^.,  para- 
lysis involving  the  various  bundles  of  the  third  nerve 
between  the  nucleus  and  the  surface  origin  of  the  nerve. 
A  distinction  between  a  nuclear  paralysis  and  a  fascicular 
paralysis  cannot  at  present  be  made,  either  in  the  case 
of  acute  or  of  chronic  lesions.  A  chronic  palsy  is  almost 
always  nuclear  and  almost  never  fascicular,  but  an  acute 
or  subacute  palsy  is  probably  as  often  fascicular  as  nuclear. 
The  involvement  of  all  the  functions  of  a  nerve  in  almost 
equal  degree  indicates  a  peripheral  lesion. 

In  cases  of  ocular  paralysis  of  chronic  development, 
the  distinction  of  a  nuclear  (or  fascicular)  from  a  periph- 
eral palsy  is  based  on  the  following  indications  : 

1.  The  exemption  of  the  intrinsic  muscles  of  the  eye. 
This  is  a  very  valuable  indication,  but  is  not  absolutely 
distinctive  of  nuclear  disease. 

2.  The  absence  or  slight  development  of  ptosis. 

3.  Bilateral  distribution  of  the  symptoms. 

4.  Irregular,  apparently  random  distribution  of  the 
paralysis. 

5.  The  association  of  chronic  ocular  palsy  with  cere- 
bral or  spinal  symptoms,  especially  symptoms  that  suggest 
a  lesion  of  a  degenerative  character. 

In  cases  where  both  the  internal  and  external  muscles 
of  both  eyes  are  paralyzed    the  diagnosis  of  a  nuclear 


THE   DIAGNOSIS    OF   CLINICAL   TYPES.  4II 

lesion  can  be  made  only  after  excluding  the  presence  of 
disease  at  the  base  of  the  brain  [jjide  Localization). 

Recurrent  Ophthalmoplegia  (Periodical  Ophthalmo- 
plegia).— In  rare  cases  there  is  observed  a  transient 
paralysis  of  ocular  muscles  (chiefly  those  supplied 
by  the  third  nerve  of  one  side),  which  makes  its 
appearance  at  long  or  short  intervals  during  a  long 
period  of  time.  The  character  of  the  attacks  varies 
somewhat  in  different  cases.  The  onset  is  rapid 
and  is  usually  attended  with  pain,  generally  severe, 
in  the  eye  affected,  and  often  there  is  unilateral 
headache  and  vomiting.  The  paroxysms  thus  closely 
resemble  attacks  of  migraine  with  ophthalmoplegia  super- 
added [vide  Migraine).  The  paralysis  is  sometimes  com- 
plete, sometimes  incomplete.  Ptosis  is  generally  present, 
and  the  intrinsic  muscles  of  the  eye  are  often  involved 
with  the  extrinsic  muscles.  The  duration  of  the  attacks 
varies  much  in  different  cases,  and  even  in  the  same  case 
at  different  times.  Usually  the  paralysis  lasts  from  two 
to  six  weeks,  its  duration  being  longest  when  the  intervals 
are  long.  The  frequency  of  the  attacks  also  varies  greatly 
in  different  cases — in  most  cases  the  interval  between  the 
paroxysms  varies  from  one  month  to  one  year. 

It  is  important  to  note  that  in  some  cases  slight  loss 
of  power  persists  during  the  intervals.  The  nature 
of  these  cases  of  recurrent  ophthalmoplegia  is  obscure, 
but  there  is  good  reason  to  believe  that  the  condition  is 
related,  in  many  ways  both  clinically  and  pathologically, 
to  migraine  (ophthalmic  migraine).  The  palsy  probably 
depends  not  on  organic  changes,  but  on  vascular  and  per- 
haps in  some  cases  on  nutritional  changes  in  the  nuclei. 

Multiple  or  Disseminated  Sclerosis.— Insular 
sclerosis  is  a  degenerative  disease  of  the  central  nervous 
system — of  the  cord  as  well  as  of  the  brain, — in  which 


412         DISEASES   OF  THE   NERVOUS   SYSTEM. 

patches  of  sclerosis  occur  irregularly  scattered  through- 
out its  white  substance.  The  favorite  seats  for  the  islets 
of  sclerosis  are  the  centrum  ovale,  crus,  pons,  medulla, 
and  cord,  but  they  may  occur  in  almost  any  part,  even 
,in  the  peripheral  nerves,  and  entail  a  corresponding 
multiplicity  in  the  characters  of  the  symptoms 

The  characteristic  and  almost  distinctive  feature  of 
insular  sclerosis  is  a  coarse  jerky  inco-ordination  {vide 
p.  103)  of  the  limbs  and  especially  of  the  arms.  This  inco- 
ordination is  present  only  during  voluntary  effort  ("  inten- 
tion tremor  or  action  tremor").  It  is  associated  usually 
from  the  beginning  with  some  loss  of  power  in  the  limbs 
affected,  and  this  loss  progresses  gradually  as  the  disease 
advances.  The  reason  why  this  combination  of  jerky 
inco-ordination  and  weakness  in  the  limbs  is  so  con- 
stantly observed  in  cases  of  disseminated  sclerosis  is  that 
the  pons  and  cord  are  very  regularly  the  seat  of  patches 
of  sclerosis,  some  of  which  almost  necessarily  involve 
some  part  of  the  motor  path. 

Associated  with  the  jerky  inco-ordination  and  weak- 
ness are  usually  a  variety  of  other  symptoms  of  less  con- 
stant occurrence.  Of  these  the  following  are  the  most 
important : 

1.  Nystagmus.  This  is  an  early  and  frequent  symptom 
(present  in  three  fourths  of  all  cases). 

2.  A  peculiar  defect  in  articulation,  consisting  usually 
of  an  undue  separation  and  accentuation  of  the  syllables 
of  words  (known  as  "  scanning  "  speech),  or  of  the  words 
of  a  sentence. 

3.  A  slight  and  variable  degree  of  mental  defect.  This 
consists  generally  of  loss  of  memory  and  an  unnatural  con- 
tentment with  the  patient's  surroundings  and  condition. 

4.  Partial  atrophy  of  the  optic  nerve  with  gradual  loss 
of  sight.     Advanced  atrophy  of  the  optic  nerve  is  met 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.         413 

with  in  only  a  small  proportion  of  the  cases,  but  a  slight 
degree  of  change  (follows  on  the  temporal  side  of  the 
disc)  is  present  in  a  very  large  number  of  cases  (vide 
page  174). 

5.  Increase  of  knee-jerks  and  of  muscle  reflexes  gener- 
ally is  observed  in  most  of  the  cases  in  which  there  is 
jerky  inco-ordination.     Babinski's  sign  is  also  present. 

In  addition  to  (or  in  place  of)  these  cardinal  symptoms 
of  insular  sclerosis,  others  of  less  frequent  occurrence 
are  observed,  among  them  loss  of  knee-jerk,  sensory  dis- 
turbances, paralysis  of  cranial  nerves — especially  the 
sixth,  seventh,  and  twelfth  nerves— headache,  vertigo, 
giddiness,  and  double  vision. 

Like  other  degenerative  diseases,  disseminated  sclerosis 
is  slowly  progressive  in  its  course,  but  it  is  not  generally 
uniformly  progressive,  for  periods  of  progress  alternate 
with  periods  during  which  the  disease  appears  stationary. 
Sometimes  in  the  course  of  the  disease  there  are  acute 
attacks  of  vertigo  and  giddiness,  associated  occasionally 
with  vomiting  and  accompanied  at  times  with  diplopia. 
After  such  an  attack  the  symptoms  of  the  disease  are 
aggravated.  These  attacks  usually  occur  early  in  the  dis- 
ease, and  they  may  be  the  first  symptoms  observed. 

Disseminated  sclerosis  may  be  confounded  with  par- 
alysis agitans,  locomotor  ataxia,  intracranial  tumor, 
general  paralysis,  primary  lateral  sclerosis,  infantile  cere- 
bral paralysis,  and  with  some  manifestations  of  hysteria. 

The  distinction  from  paralysis  agitans  is  seldom  diffi- 
cult. The  tremor  of  insular  sclerosis  is  coarse,  irregular, 
and  jerky,  and  is  present  only  during  voluntary  effort  ; 
that  of  paralysis  agitans  is  usually  regular,  rhythmical,  and 
relatively  narrow  in  range  and  is  continued  during  rest, 
except  in  rare  instances  in  the  beginning  of  the  disease. 
In  paralysis  agitans  the  parts  that  are  the  seat  of  tremor 


414         DISEASES    OF   THE   NERVOUS   SYSTEM. 

are  early  rigid  and  the  hand  assumes  a  distinctive  atti- 
tude of  flexion  which  is  absent  in  insular  sclerosis.  In 
the  cases  where  the  tremor  of  paralysis  agitans  stops 
during  rest,  the  carriage  of  the  patient,  the  facies,  the  fixed 
gaze  and  the  rigidity  are  sufficiently  distinctive.  The 
head  frequently  shares  in  the  tremor  of  insular  sclerosis; 
it  is  rarely  affected  in  paralysis  agitans.  Nystagmus  is 
common  in  insular  sclerosis,  unknown  in  paralysis  agitans. 
In  insular  sclerosis  the  speech  is  usually  "scanning"  in 
character;  in  paralysis  agitans  it  may  be  normal  or  un- 
duly rapid,  with  a  tendency  to  confluence  of  syllables, 
and  a  decided  monotony  of  voice.  It  is  very  rare  for  in- 
sular sclerosis  to  commence  after  the  fortieth  year,  while 
it  is  uncommon  for  paralysis  agitans  to  begin  before  the 
thirtieth  year.  In  cases  in  which  tremor  is  the  only 
marked  symptom  and  the  diagnosis  seems  doubtful,  the 
presence  of  optic  atrophy  (usually  slight  in  degree)  points 
to  insular  sclerosis,  and  in  less  doubtful  cases  strengthens 
the  diagnosis. 

The  distinction  from  locomotor  ataxia  is  considered 
under  the  latter  disease,  and  from  general  paralysis  of 
the  insane  under  that  title. 

A  superficial  resemblance  exists  between  cases  of  tumor 
and  insular  sclerosis  in  the  cases  where  tumor  of  the 
pons  or  crus  (see  Localization)  is  accompanied  with  wild 
jerky  inco-ordination  almost  identical  with  that  of  insular 
sclerosis.  There  the  resemblance  stops,  and  it  is  hardly 
possible  to  confound  the  other  characters  of  tumor 
(headache,  optic  neuritis,  local  spasm,  local  paralysis), 
with  the  picture  of  insular  sclerosis  that  has  been  pre- 
sented above  (combination  of  tremor  and  weakness,  with 
nystagmus,  mental  failure,  defective  articulation,  and 
optic  nerve  atrophy). 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.         415 

The  diagnosis  between  insular  sclerosis  and  primary 
lateral  sclerosis  is  considered  under  lateral  sclerosis. 

Infantile  cerebral  paralysis  (diplegic  form)  occasionally 
presents  symptoms  that  resemble  closely  those  of  insular 
sclerosis.  There  may  be  the  wild  jerky  inco-ordination 
of  the  arms  upon  voluntary  movement  that  is  so  sugges- 
tive of  insular  sclerosis.  If  the  patient  is  between  ten 
and  twenty  years  of  age,  shows  little  evidence  of  paraly- 
sis, and  only  slight  mental  failure  and  slight  speech  de- 
fect, the  distinction  from  insular  sclerosis  may  not  be 
easy.  The  most  important  help  in  making  the  diagnosis 
in  such  a  case  is  the  fact  that  in  infantile  cerebral  paraly- 
sis there  is  usually  a  history  of  trauma  during  birth,  or 
a  history  of  a  distinct  acute  onset,  with  or  without  trauma, 
or  an  acute  specific  fever  as  a  factor  after  birth,  while  in 
insular  sclerosis  there  is  the  history  of  a  gradual  develop- 
ment of  the  disease.  In  infantile  cerebral  paralysis  there 
is  further  a  history  of  distinct  paralysis  which  has  gradually 
disappeared.  If  no  history  of  the  mode  of  development 
of  the  disease  can  be  obtained  the  distinction  rests  on 
the  objective  features  of  the  case.  In  infantile  cerebral 
paralysis  (diplegic  form)  some  of  the  evidences  of  the 
former  paralysis  are  usually  present  (slight  weakness, 
difficulty  in  performing  fine  acts  with  fingers,  atrophy, 
arrest  of  development,  contractures,  etc.).  There  may  be 
some  cranial  deformity,  with  a  high  arched  palate.  The 
mental  defect  of  infantile  cerebral  paralysis  is  some  grade 
of  dementia  ;  that  of  insular  sclerosis  is  a  slighter  grade  of 
simple  mental  failure  combined  with  a  state  of  undue 
complacency.  The  presence  of  nystagmus  would  make 
the  diagnosis  of  insular  sclerosis  certain. 

It  is  more  common  for  insular  sclerosis  to  be  mistaken 
for  hysteria  than  for  the  opposite  error  to  be  made,  but 


4l6        DISEASES   OF   THE   NERVOUS   SYSTEM. 

each  mistake  is  occasionally  made.  Insular  sclerosis  may 
be  mistaken  for  hysteria  when  the  former  disease  occurs, 
as  it  frequently  does,  in  young  women  who  present  some 
actual  symptoms  of  hysteria/  Generally  this  error  is 
avoidable.  The  mere  fact  of  the  existence  of  nystagmus 
indicates  that  the  condition  is  not  purely  hysterical  and 
strongly  suggests  organic  disease.  Sometimes  there  occurs 
in  hysteria  an  intention  tremor,  irregular  in  character, 
and  thus  resembling  that  of  insular  sclerosis,  but  differing 
from  it  in  being  much  narrower  in  range  and  more  rapid, 
and  in  being  associated  with  distinct  voluntary  rigidity  of 
the  antagonistic  muscles  involved.  It  is  usually  easy  to 
recognize  the  combination  of  the  symptoms  of  the  two 
diseases  when  this  exists,  but  it  may  be  impossible  to  say 
whether  certain  symptoms  belong  to  the  account  of  the 
insular  sclerosis  or  to  that  of  the  hysteria.  Thus,  in  a  case 
presenting  spastic  paralysis  of  the  lower  extremities,  un- 
certain gait,  nystagmus,  scanning  speech  and  partial 
atrophy  of  the  optic  nerve,  all  these  symptoms  would  be 
explicable  by  the  supposition  of  an  insular  sclerosis,  but 
if  there  existed  a  persistent  rhythmical  tremor  of  one 
upper  extremity  combined  with  these  symptoms  it  would 
be  plain  that  this  was  not  dependent  on  the  organic  dis- 
ease but  on  an  associated  functional  disturbance — /*.  e., 
that  it  was  of  hysterical  origin.  If,  however,  there  also 
existed  in  this  instance  concentric  limitation  of  the  visual 
fields  and  loss  of  sensibility  of  the  extremities  it  would 
be  difficult  or  impossible  to  fix  on  the  correct  interpre- 
tation of  these  symptoms,  since  they  might  be  referable 
either  to  the  organic  or  to  the  functional  disturbance. 

Bulbar     Paralysis. — Progressive    bulbar    or    glosso- 
labio-laryngeal  paralysis  is  a  chronic  degenerative  disease 

'  Probably  no  organic  disease  of   the  brain  is  so  apt  to  have  asso- 
ciated with  it  some  manifestations,  slight  or  considerable,  of  hysteria. 


THE  DIAGNOSIS  OF  CLINICAL  TYPES.         417 

of  certain  nuclei  of  the  medulla  oblongata.  Its  symp- 
toms depend  on  the  locality  of  the  lesion  and  as  this  is 
usually  the  same,  the  manifestations  of  the  disease  are 
reasonably  constant.  The  great  characteristic  of  the  con- 
dition is  a  slowly  progressive  and  strictly  bilateral  paralysis 
of  the  tongue,  lips,  palate,  pharynx,  and  frequently  of  the 
larynx,  often  associated  with  visible  wasting  of  the  tongue 
and  lips.  The  effect  of  this  paralysis  is  to  cause  :  (i)  im- 
perfect articulation  of  sounds  in  which  the  tongue  plays 
an  important  role — especially  lingual  consonants,  /,  n,  r, 
and/y  and  (2)  difficulty  in  swallowing,  from  weakness 
of  the  pharynx  and  palate. 

After  a  period  which  varies  in  different  cases  from  one 
to  several  years  from  the  commencement  of  the  disease, 
the  patient  falls  into  a  characteristic  condition  of  partial 
helplessness,  from  the  progress  of  the  above  mentioned 
paralysis.  In  this  terminal  state  the  tongue  lies  motion- 
less, the  saliva  dribbles  from  the  open  mouth,  the  lower 
part  of  the  face  is  without  expression  and  articulate  speech 
is  impossible.     The  intellect  remains  perfectly  clear. 

Not  uncommonly  chronic  bulbar  paralysis  is  associated 
with  chronic  degenerative  processes  in  other  parts.  Of 
these  associations  the  most  common  is  progressive  muscu- 
lar atrophy  (see  p.  446).  In  some  cases  the  bulbar 
symptoms,  in  others  the  spinal  symptoms,  make  their 
appearance  first  and  are  chiefly  conspicuous. 

Besides  this  chronic  progressive  type  of  bulbar  paralysis 
there  are  two  other  clinical  forms  of  bulbar  paralysis. 
These  forms  resemble  the  chronic  form  in  presenting  the 
same  combination  of  glosso-labio-laryngeal  paralysis  of 
symmetrical  distribution,  but  differ  from  it  in  being  of 
sudden  or  rapid  onset.  The  similarity  in  distribution  of 
symptoms  depends  on  a  similarity  in  the  position  of  the 
lesion  ;  the  difference  in  the  onset  depends  on  a  difference 


41 8        DISEASES   OF  THE   NERVOUS   SYSTEM. 

in  the  nature  of  the  lesion.     In  both  the  forms  mentioned 
the   lesion  is  a  vascular  lesion  ;  in  one  it  is  hemorrhage, 
in  the    other   inflammation.     In  the   first   form    (hemor- 
rhagic)^ the    symptoms    come    on    suddenly,  often    with 
vomiting  and  giddiness,  but  usually  without  loss  of  con- 
sciousness.    At  first  there  may  be  some  loss  of  power  in 
the  limbs   and  perhaps    some    sensory    disturbance,  but 
this  wears  rapidly  away,  leaving  behind  a  stationary  con- 
dition of  glosso-labio-laryngeal  paralysis.     In  the  second 
form  (inflammatory),^  which  is  much  more  rare  than  the 
first,   the   symptoms  come   on   rapidly  (acutely)  but  not 
suddenly,  and  are  accompanied  with  fever,  vomiting,  etc.^ 
The  diagnosis  of  chronic  bulbar  paralysis  is  usually 
not  difficult,  for  the  distribution  of  the  paralysis,  with  its 
bilateral     symmetry   and    slowly   progressive   course,    is 
highly  distinctive.     A  tumor  outside  the  medulla,  dama- 
ging the  nerve-roots,  or  in  the   substance  of  the  medulla, 
may  cause  bulbar  symptoms   of  slow    onset    resembling 
those  of  the  degenerative  disease.     The  diagnosis  is  based 
on    the    fact   that  tumors   in  either   of    these    situations 
usually  produce  unilateral   symptoms,  or  if  they  produce 
bilateral  symptoms  these  have  not  the  highly  symmetrical 
distribution  that  distinguishes  chronic  bulbar  paralysis. 
In  tumor,  again,  there  is  usually  headache,  and  often  con- 
vulsions,  and  sometimes   optic  neuritis,  all  of  which  are 
absent    in  chronic  bulbar  paralysis.     The  age  at  which 

'  These  are  simply  cases  of  hemorrhage  into  the  medulla,  which  arc 
symmetrical  and  occupy  the  same  nuclei  as  are  affected  in  the  degen- 
erative  process.  Much  more  often  hemorrhage  into  the  medulla  is  a 
random  process. 

^  These  cases  are  allied  to  cases  of  acute  poliomyelitis. 

^  Neither  form  is  of  course  to  be  regarded  as  a  distinct  disease, 
for  the  same  processes  that  cause  them  are  much  more  common  io 
other  regions. 


THE  DIAGNOSIS   OF  CLINICAL  TYPES.  419 

chronic  bulbar  paralysis  occurs  may  help  in  the  diagnosis, 
for  tumors  are  not  frequent  after  the  fiftieth  year,  while 
chronic  bulbar  paralysis  seldom  commences  before  this 
time. 

Symmetrical  lesions  in  the  motor  paths  of  both  hemi- 
spheres may  give  rise  to  symptoms  resembling  those  of 
bulbar  paralysis,  bilateral  paralysis  of  tongue,  lips  and 
pharynx — "  pseudo-bulbar  paralysis  "  it  is  called.  When 
such  symptoms  depend  on  acute  lesions  (hemorrhage, 
softening),  as  they  usually  do,  the  diagnosis  is  easy. 
When  they  depend  on  chronic  lesions  (tumor,  chronic 
meningitis),  the  distinction  may  be  more  difficult,  and  is 
then  based  chiefly  on  the  fact  that  in  these  cases  there 
are  usually  evidences  of  involvement  of  other  parts  than 
the  tongue,  lips  and  pharynx,  (face,  arm,  leg) — that  there 
is  in  fact,  or  has  been,  a  double  hemiplegia.  Another 
point  of  distinction  is  that  in  these  cases  there  is  no 
atrophy  of  the  lips  and  tongue,  and  that  reflex  action 
of  the  pharynx  is  never  impaired.  But  these  are  not 
absolute  criteria. 

General  Paralysis  of  the  Insane  (General  Paresis 

or  Paralytic  Dementia). — The  symptoms  of  general 
paralysis  of  the  insane  are  exceedingly  varied,  but  in  all 
cases  there  are  present  evidences  of  both  mental  and 
physical  derangement.  Sometimes  the  mental  symptoms, 
sometimes  the  physical  symptoms,  are  first  prominent. 
Either  set  of  symptoms  may  be  especially  obtrusive 
during  the  course  of  the  disease,  or  both  sets  may  be 
equally  conspicuous. 

The  mental  symptoms  that  are  most  characteristic  are 
as  follows: 

I.  Loss  of  mental  power,  as  shown  by  defective  atten- 
tion, defective  memory,  clouded  consciousness,  impair- 


420        DISEASES   OF  THE   NERVOUS   SYSTEM. 

ment  of  judgment,  and  early  mental  fatigue  in  the  per- 
formance of  ordinary  duties. 

2.  Change  in  character,  as  shown  by  irritability,  in- 
difference to  the  wants  or  sufferings  of  others  as  well  as 
to  personal  interests,  defective  will  power,  with  partial  or 
entire  loss  of  moral  sense,  and  silly  fabrications. 

3.  Unsystematized  and  varying  delusions,  especially 
delusions  of  grandeur,  in  which  the  patient  believes  him- 
self to  be  some  celebrated  personage  (^.^.,  Napoleon, 
Caesar,  Christ),  or  to  be  possessed  of  enormous  wealth,  or 
of  great  personal  strength,  etc.  These  exaggerated  and 
variable  personal  delusions  are  not  usually  present  during 
the  earliest  periods  of  the  disease,  but  are  rarely  absent 
after  it  has  become  established.  They  are  always  associ- 
ated with,  and  generally  preceded  by,  a  period  in  which 
the  patient  has  an  exalted  sense  of  well-being,  which, 
when  present,  is  highly  characteristic.  Less  than  one 
third  of  the  cases  present  the  state  of  typical  exaltation. 
Depressing  delusions  are  quite  as  often  met  with  as  ex- 
pansive ideas.  As  a  matter  of  convenience  in  more 
exact  clinical  description,  the  demented,  agitated,  de- 
pressed, and  expansive  forms  of  the  disease  are  diag- 
nosticated. Side  by  side  with  these  mental  changes  are 
developed  a  series  of  physical  phenomena  of  which  the 
most  distinctive  are  as  follows  : 

1.  Hesitating  and  monotonous  speech  with  a  tendency 
to  slur  the  endings  of  words. 

2.  Tremor  on  voluntary  movement,  especially  marked 
in  the  upper  extremities  and  in  the  lips  during  articu- 
lation ;  fibrillary  tremor  in  the  tongue  when  protruded, 
and  in  the  muscles  of  the  face  during  speech  or  during 
excitement. 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.         42 1 

3.  Pupillary  changes,  especially  marked  inequality, 
myosis,  and  loss  of  light  reaction. 

4.  Exaggeration  of  the  wrist-,  elbow-,  and  knee-jerks. 
The  symptoms  above  enumerated  are  very  constant,  the 

majority  of  them  making  their  appearance  in  all  cases  of 
general  paralysis.  In  addition  to  these  there  are  others 
of  considerable  importance  that  are  much  less  constant, 
but  are  liable  to  make  their  appearance  at  almost  any 
period  of  the  disease.  These  symptoms  are  both  mental 
and  physical,  and  comprise  the  following  phenomena  : 

1.  Melancholia  or  hypochondriasis,  in  which  headache 
is  prominent.     These  are  usually  early  symptoms. 

2.  Maniacal  outbreaks. 

3.  Sudden  epileptiform  attacks. 

4.  Apoplectiform  seizures  characterized  by  sudden 
loss  of  consciousness  and  hemiplegic  symptoms,  which 
latter  usually  disappear  quickly. 

In  about  six  per  cent,  of  the  cases  the  symptoms  of 
posterior  sclerosis  are  combined  with  the  symptoms  of 
general  paralysis  {vide  p.  462).  In  such  cases  the  knee- 
jerks  are  lost  instead  of  being  exaggerated,  there  are 
lightning  pains,  and  ataxia  is  a  prominent  symptom. 

General  paralysis,  like  other  progressive  degenerative 
diseases,  is  not  uniformly  progressive.  Periods  of  re- 
mission, often  of  considerable  duration,  alternate  with 
periods  of  progress,  but  there  are  great  differences  in  the 
duration  of  the  disease  (one  to  six  years).  In  all  cases 
where  death  does  not  occur  in  the  acute  stages  of  the 
disease  (apoplectic  attacks),  or  from  intercurrent  disease, 
their  termination  is  in  complete  dementia  and  physical 
helplessness.  In  a  fully  developed  case  of  general  paraly- 
sis there  are  practically  no  difficulties  in  diagnosis;  the 


422         DISEASES   OF   THE   NERVOUS   SYSTEM. 

conspicuous  mental  failure  and  characteristic  expansive 
or  depressive  delusions,  in  combination  with  tremor, 
speech  disturbance,  etc.,  make  the  nature  of  the  disease 
only  too  evident.  In  the  early  stages  of  the  affection 
the  case  is  very  different;  the  symptoms  may  be  so 
equivocal  that  a  positive  diagnosis  is  not  possible. 
The  conditions  with  which  general  paralysis  may  be 
confounded  are:  (i)  neurasthenia,  (2)  chronic  alco- 
holism, (3)  chronic  meningitis,  (4)  tremor,  (5)  cerebral 
lues,  (6)  senile  dementia,  and  (7)  the  sequelae  of  sun- 
stroke. The  diagnosis  from  neurasthenia  may  be  impos- 
sible at  an  early  period,  but  a  diagnosis  can  generally  be 
made  when  the  patient  is  first  seen  by  the  physician. 
In  neurasthenia  there  may  be  some  mental  failure — loss 
of  memory,  defective  attention,  etc.,  and  there  may  be 
tremor  in  the  upper  extremities,  but  the  mental  failure 
is  never  so  considerable  in  degree  as  in  general  paralysis, 
and  the  patient  is  not  only  conscious  of  its  existence  but 
exaggerates  its  importance,  while  in  general  paralysis  he 
is  only  rarely  cognizant  of  the  existence  of  any  mental 
weakness.  The  neurasthenic  is  able  to  concentrate  his 
attention  sufficiently  to  write  correctly  at  dictation.  The 
general  paralytic  is  frequently  unable  to  do  this  ;  he  omits 
letters  or  transposes  them  in  a  way  that  indicates  defective 
attention,  although  he  may  be  making  a  pronounced  effort 
to  write  correctly.  If  in  addition  to  mental  weakness  and 
irritability  there  is  speech  disturbance  and  tremor  on 
movement  of  hand  and  lips,  there  is  a  strong  presumption 
that  the  condition  is  general  paralysis  and  not  neurasthe- 
nia, and  this  is  true  a  fortiori^  if  there  is  evidence  of 
delusions  or  if  there  are  immobile  pupils. 

Hydrocephalus  (Dropsy  of  the  Brain). — The  word 
hydrocephalus  is  employed  to  designate  an  accumulation 


THE  DIAGNOSIS   OF   CLINICAL  JYPES.         423 

of  serous  fluid  within  the  skull.  When  the  accumulation 
is  in  the  arachnoid  space  the  condition  is  termed  external 
hydrocephalus  ;  when  within  the  ventricles,  internal  hy- 
drocephalus. Hydrocephalus  may  run  an  acute  or  chronic 
course,  may  be  congenital  or  acquired,  and  may  be  ap- 
parently primary  or  distinctly  dependent  on  some  other 
morbid  process. 

Acute  Hydrocephalus  is  usually  dependent  on  tuber- 
cular meningitis,  and  owing  to  the  frequency  with  which 
some  degree  of  serous  accumulation  accompanies  cases 
of  meningitis  the  terms  acute  hydrocephalus  and  menin- 
gitis have  been  used  synonymously.  Clinically  acute 
hydrocephalus  is  of  secondary  importance  to  the  menin- 
gitis on  which  it  depends  and  of  which  it  is  merely 
one  symptom.  The  serous  effusion  depends,  in  acute 
hydrocephalus,  on  inflammation  of  the  pia,  ependyma, 
and  choroid  plexuses. 

Chronic  External  Hydrocephalus  is  a  condition  of  little 
clinical  interest  and  may  be  passed  by.  Chronic  Internal 
Hydrocephalus,  on  the  other  hand,  is  a  condition  of  fre- 
quent occurrence  and  considerable  importance.  It  occurs 
as  a  congenital  and  as  an  acquired  condition.  Congenital 
internal  hydrocephalus  develops  during  intra-uterine  life. 
After  birth  the  cranium  enlarges  rapidly,  the  face  remain- 
ing of  normal  size.  The  fontanelles  become  large  and 
prominent,  the  sutures  separate  widely  and  the  cranium 
attains  a  characteristic  globular  form.  There  is  usually 
much  mental  defect.  Death  usually  occurs  after  a  few- 
months,  but  in  some  instances  the  process  becomes  sta- 
tionary and  the  patient  reaches  adult  life,  though  with 
considerable  mental  weakness  and  perhaps  disorders  of 
motion. 

The  acquired  form  of  chronic  internal  hydrocephalus 


424         DISEASES   OF  THE  NERVOUS  SYSTEM. 

usually  occurs  without  known  cause.  Sometimes,  how- 
ever, it  is  apparently  secondary  to  a  morbid  process  which 
causes  effusion  mechanically  by  the  obliteration  of  the 


FIG.  48. 
Hydrocephalus  and  Meningocele. 

openings'  through  which  the  ventricular  fluid  ordinarily 
passes.    Tumors,  chronic  syphilitic  meningitis  and  acute 

'  It  is  thought  that  closure  of  the  openings  in  the  membrane  closing 
the  fourth  ventricle  from  the  subarachnoid  space  is  the  most  import- 
ant mechanical  cause  of  hydrocephalus,  but  the  entire  subject  of  causa- 
tion is  involved  in  obscurity. 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.         425 

meningitis  are  the  chief  conditions  by  which  this  result  may 
be  brought  about.  Both  primary  and  secondary  forms'  of 
acquired  chronic  internal  hydrocephalus  occur  in  chil- 
dren and  in  adults.  In  children  the  symptoms  are  much 
the  same  as  in  the  congenital  form.  In  adults  there  are 
no  distinctive  symptoms. 

A  positive  diagnosis  of  hydrocephalus  can  be  made 
only  in  cases  where  there  is  decided  and  progressive  en- 
largement of  the  cranium,  and  in  such  cases  there  is  rarely 
any  diagnostic  difficulty.  When  the  enlargement  of  the 
cranium  is  not  considerable  hydrocephalus  may  be  con- 
founded with  the  enlargement  of  the  head  that  occurs  in 
rickets.  The  head  in  hydrocephalus  has  a  globular  form, 
and  the  fontanelles  are  always  tense.  In  the  typical 
rachitic  head  the  cranium  has  a  pyramidal  shape,  there 
is  no  bulging  of  the  fontanelles  and  other  evidences 
of  rickets  are  plain  enough.  It  must  not  be  forgotten, 
however,  that  many  cases  of  rickets  are  associated  with 
hydrocephalus, — the  nature  of  the  relation  between  the 
rachitic  and  the  hydrocephalic  process  being  but  imper- 
fectly understood, — and  cases  occur  in  which  it  is  difficult 
to  determine  the  true  character  of  the  head  enlargement. 
The  most  important  indication  of  a  hydrocephalic  process 
is  the  rapidity  of  the  cranial  enlargement  and  the  existence 
of  a  bulging  fontanelle.  When  the  bones  are  firmly  united, 
as  in  adults,  the  diagnosis  of  hydrocephalus  is  extremely 
difficult  and  usually  impossible.  A  positive  diagnosis  is 
possible  only  in  the  rare  cases  in  which  there  is  distinct 
enlargement  of  the  head  and  separation  of  the  sutures. 
But  in  the  absence  of  such  enlargement  hydrocephalus  may 
perhaps  be  suspected  if  mental  weakness,  somnolence, 
coma,  convulsions,  loss  of  power,  etc.,  follow  very  slowly 
on  one  or  more  attacks  of  acute  meningitis.  In  very  rare 
instances  general  thickening  of  the  cranial  bones  may  be 


426         DISEASES   OF  THE   NERVOUS   SYSTEM. 

confounded  with  the  enlargement  of  the  head  that  occurs 
in  hydrocephalus.  External  and  internal  hydrocephalus 
may  sometimes  be  distinguished  by  the  introduction 
of  an  exploring  syringe  and  the  withdrawal  of  fluid 
in  the  former  case  from  the  arachnoid  space,  in  the 
latter  from  the  ventricles,  but  even  this  method  is  not 
infallible. 

Diseases  of  the  Spinal  Cord. 

Spinal  Meningitis. — The  individual  symptoms  of 
spinal  meningitis  vary  considerably  in  distribution,  ac- 
cording to  the  position  of  the  disease,  and  in  their  char- 
acter, according  to  the  acuteness  of  the  process.  In  most 
cases  there  are  present  certain  local  symptoms,  as  pain, 
spasm,  rigidity,  hypersesthesia,  anaesthesia,  motor  paraly- 
sis, etc.,  and  it  is  convenient  to  think  of  these  symptoms 
according  as  they  are  due  (i)  to  irritation  of  the  mem- 
branes, (2)  to  irritation  of  the  nerve-roots,  (3)  to  com- 
pression of  the  nerve-roots,  or  (4)  to  compression  of  the 
cord.  The  chief  symptom  of  irritation  of  the  inflamed 
membranes  is  pain  in  the  back,  usually  constant  and  in- 
creased by  movement.  The  chief  indication  of  irritation 
of  the  nerve-roots  are  radiating  pains  and  hyperaesthesia 
from  irritation  of  sensory  (posterior)  roots,  and  rigidity 
and  spasm  or  contractures  from  irritation  of  the  motor 
(anterior)  roots.  When  the  nerve-roots  are  compressed 
instead  of  irritated,  there  are  analgesia  and  anaesthesia 
instead  of  pain  and  hyperaesthesia,  and  muscular  paralysis 
and  relaxation  in  place  of  rigidity  and  spasm.  If  the 
compression  of  the  nerve-roots  is  considerable  there  are 
trophic  changes  (atrophy)  in  the  muscles  paralyzed,  with 
loss  of  reflex  action.  The  symptoms  of  involvement  of 
the  cord  by  pressure  resemble  those  of  a  transverse  lesion 
of  the  cord  {vide  page    245)  :   paralysis   of  motion   and 


THE    DIAGNOSIS    OF   CLINICAL   TYPES.         427 

sensation  below  the  level  of  the  lesion,  increased  reflex 
action,  etc. 

It  is  convenient  to  distinguish  the  following  clinical 
forms  of  spinal  meningitis  : 

(i)  External  meningitis,  (2)  Internal  meningitis,  (a) 
Acute,  (^)  Chronic. 

External  Meningitis  {Yj^\qxx\2\  Spinal  Pachymeningitis). 
— External  meningitis  is  probably  secondary,  in  all  cases, 
to  adjacent  disease,  and  the  particular  form  of  disease 
to  which  it  is  almost  invariably  secondary  is  caries  of  the 
spine  (Pott's  disease). 

The  symptoms  of  the  disease  vary  considerably,  ac- 
cording as  the  process  runs  an  acute  or  chronic  course, 
and  also  according  as  the  symptoms  of  caries  (its  usual 
cause)  are  obtrusive  or  inconspicuous. 

In  acute  cases  the  symptoms  of  external  pachymenin- 
gitis closely  resemble  those  of  internal  meningitis  {vide 
internal  meningitis).  In  such  cases  the  following  are 
the  chief  indications  of  the  disease  : 

1.  Pain  in  the  back,  increased  by  movement. 

2.  Rigidity  of  the  muscles  of  the  spine. 

3.  Radiating  pains  in  the  extremities,  with  or  without 
spasm. 

4.  Hypersesthesia  of  the  skin. 

5.  Fever,  often  considerable  in  degree. 

These  symptoms  may  exist  alone,  or  may  be  combined 
with  symptoms  of  pressure  or  inflammation  of  the  cord 
itself,  especially  paraplegia  or  paraplegic  weakness,  and 
excessive  reflex  action  in  the  lower  extremities  when  the 
pressure  is  above  the  lumbar  enlargement. 

The  symptoms  indicating  a  more  chronic  process  dif- 
fer from  those  above  enumerated  chiefly  in  the  absence 
of  considerable  fever  and  in  the  less  obtrusive  character 
of  the  irritative  symptoms,  especially  muscular  rigidity 


428         DISEASES   OF   THE   NERVOUS   SYSTEM. 

and  spasm.  In  very  chronic  cases  there  are  no  distinc- 
tively meningitic  symptoms.  The  symptoms  are  those 
of  the  bone  disease.  The  distinction  of  external  menin- 
gitis from  internal  meningitis  is  impracticable  from  the 
symptoms  alone.  In  order  to  establish  the  diagnosis  it 
is  necessary  to  consider  the  etiology  of  the  affection 
with  much  care,  with  a  view  to  discovering  evidence  of 
a  condition  to  which  the  meningitis  may  be  secondary. 
The  presence  of  caries  of  the  spine  makes  the  diagnosis 
certain  ;  but  as  it  is  easy  to  overlook  the  slighter  evi- 
dences of  such  disease  (local  tenderness,  irregularity  of 
the  spines),  caries  cannot  be  positively  excluded  unless 
the  spine  has  been  repeatedly  and  carefully  examined, 
including  examination  by  the  X-rays.  In  the  majority 
of  cases  of  external  meningitis  the  evidences  of  caries 
are  sufficiently  distinct  to  enable  the  diagnosis  of  the 
character  of  the  meningeal  affection  to  be  made;  in  a 
few  cases  only  is  the  diagnosis  impossible. 

Acute  Internal  Meningitis. — The  symptoms  that  point 
to  the  existence  of  acute  internal  meningitis  are  essen- 
tially those  of  the  acute  form  of  external  meningitis 
already  described  (p.  403)  :  pain  in  the  back,  rigidity  "of 
the  muscles  of  the  spine,  radiating  pains  in  the  extrem- 
ities, with  hyperaesthesia,  and  spasm  brought  on  espe- 
cially by  movement.  The  onset  of  these  symptoms 
is  acute,  and  is  generally  attended  with  fever,  sometimes 
by  rigors.  The  grouping  of  the  symptoms  enumerated 
varies  with  the  situation  of  the  disease.  When  the 
meninges  of  the  lumbar  region  are  chiefly  involved,  the 
pain  and  spasm  and  hyperaesthesia  are  confined  to  the 
lower  extremities.  When  the  dorsal  meninges  are  chiefly 
affected,  the  symptoms  extend  to  the  muscles  and  skin 
of  the  trunk.  When  the  cervical  meninges  are  the  seat 
of  the  disease  the  symptoms  affect  the  arms,  and  there 


THE   DIAGNOSIS    OF   CLINICAL   TYPES.  429 

may  be  bulbar  symptoms,  as  dyspnoea  and  difficult 
swallowing. 

Acute  internal  spinal  meningitis  may  be  complicated 
by  cerebral  meningitis,  or  the  symptoms  of  cerebral 
meningitis  may  precede  those  of  the  spinal  disease.  The 
symptoms  indicating  extension  to  the  cerebral  meninges 
are  vomiting,  headache,  delirium  and  paralysis  of 
cranial  nerves  {vide  acute  meningitis).  The  character 
of  the  inflammation,  whether  purulent  or  tubercular,  does 
not  entail  any  distinctive  difference  in  the  character  of 
the  symptoms.  The  duration  of  the  acute  symptoms 
varies  from  a  few  days  (severe  cases)  to  several  weeks. 
In  cases  that  recover,  or  in  which  death  does  not  occur 
early,  the  symptoms  grow  gradually  less  acute.  This 
subacute  stage  may  endure  for  months,  and  may  pass 
into  a  chronic  stage. 

The  etiology  of  acute  internal  spinal  meningitis  does 
not  usually  give  much  help  in  the  diagnosis  of  the  affec- 
tion. The  disease  may  follow  exposure  to  cold,  over- 
exertion, trauma,  sunstroke,  acute  febrile  diseases,  septi- 
caemia, etc.,  but  the  influence  of  some  of  these  factors  is 
uncertain,  and  all  of  them  are  related  to  many  other  con- 
ditions of  the  nervous  system  besides  meningitis.  The 
principal  affections  of  the  nervous  system  from  which 
acute  internal  spinal  meningitis  must  be  distinguished 
are  acute  myelitis,  cerebro-spinal  meningitis,  meningeal 
hemorrhage  and  tetanus.  In  acute  myelitis  paraplegia 
occurs  early  ;  in  meningitis  it  is  absent,  and  there  is  at 
first  little  or  no  motor  weakness  of  any  kind.  Moreover, 
the  spasm  of  the  limbs  and  pain  in  the  back,  which  occur 
in  meningitis,  are  not  present,  although  there  is  often  rigid- 
ity of  the  limbs  in  the  later  stages  of  myelitis  if  the  lesion 
is  above  the  lumbar  enlargement.  When  meningitis  and 
myelitis  coexist,  the  decision   into   which   category   the 


430         DISEASES   OF   THE   NERVOUS   SYSTEM. 

condition  belongs  must  depend  on  the  greater  obtrusive- 
ness  of  the  cord  symptoms  on  the  one  hand,  or  of  the 
meningeal  symptoms  on  the  other,  and  upon  the  order 
in  which  these  symptoms  have  made  their  appearance. 
The  distinction  from  meningeal  hemorrhage  is  given 
under  this  disease  (p.  409).  The  diagnosis  from  tetanus 
depends  on  the  occurrence  in  meningitis  of  fever  at  the 
onset,  and  of  marked  sensory  symptoms,  and  on  the 
occurrence  in  tetanus  of  trismus  and  the  ready  excitation 
of  spasms  by  peripheral  impressions. 

Chronic  I?iter?tal  Meningitis.  —  The  symptoms  of 
chronic  internal  meningitis,  like  those  of  acute  internal 
meningitis,  depend  on  meningeal  irritation,  on  irritation 
and  pressure  of  the  nerve-roots,  and  on  damage  to  the 
cord  itself.  The  character  of  the  symptoms  varies  much 
in  different  cases,  according  as  one  or  other  of  these 
mechanisms  in  the  production  of  the  symptoms  is  pre- 
dominant. 

In  the  majority  of  cases  the  following  are  the  symp- 
toms observed  in  chronic  internal  meningitis  : 

At  first — I.  Pain  or  discomfort  in  the  back. 

2.  Stiffness  of  the  muscles  of  the  back  (retraction  of 
the  head  when  the  meningitis  is  cervical). 

3.  Radiating  pains  in  the  arms,  legs,  or  trunk,  accord- 
ing to  the  position  of  the  disease. 

4.  Hyperaesthesia. 

Followed  by — 5.  Loss  of  sensation  in  the  regions  for- 
merly hyperaesthetic. 

6.  Weakness  in  the  muscles  formerly  rigid,  with 
atrophy. 

7.  Diminished  pain. 

8.  Symptoms  of  compression  of  the  cord  {vide  p.  420). 
In  cases  where  the  process  of  disease  affects  mainly  the 

pia  mater  (chronic  leptomeningitis),  the  symptoms  that 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.         43 1 

are  due  to  meningeal  irritation  are  especially  conspicu- 
ous, /.  (f.,  there  is  marked  pain  in  the  back,  the  radiating 
pains  are  severe,  and  rigidity  and  hypersesthesia  are 
prominent  symptoms.  The  cord  itself  may  be  in- 
volved in  these  cases,  as  shown  by  paraplegic  weak- 
ness, etc. 

In  the  cases  where  the  inflammatory  process  affects 
chiefly  the  internal  surface  of  the  dura  mater  (chronic 
internal  pachymeningitis,)  the  symptoms  that  depend  on 
involvement  of  the  nerve-roots  passing  through  the  dura 
are  especially  obtrusive.  There  are  at  first  severe  radi- 
ating pains,  spasm  and  hyperaesthesia  from  irritation, 
and  later  muscular  weakness  and  muscular  atrophy  from 
pressure  of  the  nerve-roots. 

When  the  seat  of  the  disease  is  the  cervical  region 
("  cervical  hypertrophic  pachymeningitis  "),  as  it  some- 
times is,  the  irritative  symptoms  consist  chiefly  of  pains 
in  the  arms,  shoulders  and  neck,  and  these  are  followed 
by  muscular  atrophy,  often  extensive,  in  the  arms,  and 
by  paraplegic  weakness  below  this  level,  from  cord 
pressure. 

The  etiology  of  chronic  internal  meningitis  is  usually 
too  obscure  to  be  of  much  aid  in  diagnosis.  It  is  im- 
portant to  remember,  however,  that  the  disease  some- 
times follows  chronic  alcoholism,  syphilis,  long  exposure 
to  cold  and  traumatisms,  and  also  that  it  may  be  a  sequel 
of  the  acute  form  of  spinal  meningitis,  and  hence  must 
own  the  same  causes. 

In  the  cases  of  chronic  meningitis  where  irritative 
symptoms  predominate,  the  condition  may  be  confounded 
with  muscular  rheumatism  and  rachialgia,  or,  if  the  men- 
ingitis is  of  the  lumbar  region,  with  locomotor  ataxia. 
The  resemblance  to  muscular  rheumatism  is  never  more 
than  superficial.    In  both  conditions  there  may  be  periph- 


432         DISEASES   OF  THE   NERVOUS   SYSTEM. 

eral  pains,  but  in  muscular  rheumatism  there  is  never 
the  spinal  pain,  the  hypersesthesia,  or  the  rigidity  that 
characterizes  chronic  meningitis.  The  resemblance  to 
rachialgia  may  be  closer  ;  spinal  pain  and  rigidity  of  the 
muscles  of  the  back  are  common  to  both  conditions.  In 
rachialgia,  however,  there  is  tenderness  of  a  large  part 
of  the  spine,  and  there  are  often  local  points  of  great 
tenderness  along  the  spine.  On  the  other  hand  the 
rigidity  and  radiating  pains  of  meningitis  are  absent 
in  rachialgia. 

When  chronic  meningitis  affects  the  cervical  region, 
the  rigidity  of  the  muscles  which  it  causes,  and  the  pain, 
may  be  mistaken  for  wry-neck.  In  wry-neck  the  head 
is  fixed  by  muscles  that  are  in  spasm.  In  chronic  men- 
ingitis the  head  is  fixed  owing  to  the  pain  to  which 
movement  gives  rise. 

The  chronic  localized  pachymeningitis  which  so  often 
results  from  bone  disease  has  many  symptoms  in  com- 
mon with  chronic  internal  meningitis,  and  the  distinction 
can  be  made  only  by  discovering  a  cause  of  external 
meningitis.  In  every  case  of  chronic  meningitis  the 
evidences  of  bone  disease,  local  tenderness  of  the  spine 
and  deformity,  should  be  carefully  sought  for. 

Intra-Spinal  Hemorrhage. — i.  Hemorrhage  into 
the  meninges  of  the  cord. 

2.  Hemorrhage  into  the  spinal  cord. 

Meningeal  Hemorrhage. — The  symptoms  of  hemor- 
rhage into  the  membranes  of  the  cord  are  much  the 
same  whether  the  hemorrhage  is  within  the  dura  mater 
or  external  to  it.  In  either  case  there  is  considerable 
irritation  of  the  meninges  and  nerve-roots  at  the  level  of 
the  lesion.  In  consequence  there  are  the  following  irri- 
tative symptoms  :  (i)  Severe  pain  in  the  back  ;  (2) 
radiating  pains  in  the  nerves  coming  from  the  region  of 


THE  DIAGNOSIS   OF   CLINICAL  TYPES.         433 

the  meninges  involved  ;  (3)  muscular  spasm,  which  may 
include  local  or  general  convulsions.  These  symptoms 
resemble  closely  the  symptoms  of  acute  spinal  menin- 
gitis, but  differ  from  them  in  one  important  respect,  /.  e.^ 
they  are  always  sudden  and  often  violent  in  their  onset. 

In  many  cases  paralytic  symptoms  follow  very  quickly 
upon  these  irritative  symptoms,  in  consequence  of  pres- 
sure upon  the  cord  itself.  In  such  instances  there  is  some 
loss  of  power  and  anaesthesia  below  the  level  of  the 
lesion,  with  increased  reflexes  if  the  pressure  is  located 
above  the  lumbar  enlargement.  The  paraplegia  is  rarely 
complete. 

The  precise  distribution  of  the  symptoms  enumerated 
varies  with  the  level  of  the  lesion  (page  245).  When 
this  is  in  the  cervical  region,  the  pains  are  in  the  arms 
and  neck,  there  is  retraction  of  the  head,  and  there  may 
be  evidences  of  interference  with  the  functions  of  the 
medulla — embarrassed  respiration,  dysphagia,  mydriasis, 
etc.  If  the  dorsal  region  is  involved,  there  are  severe 
pains  about  the  chest  or  abdomen.  When  the  lumbar 
meninges  are  the  seat  of  the  hemorrhage  the  pains  are 
in  the  legs  and  there  is  diminished  Sensation  and  loss  of 
power  in  the  legs,  loss  of  patellar  reflex  and  sphincteric 
weakness.  If  the  cauda  equina  is  involved,  there  are 
often  characteristic  localizing  symptoms  {vide  page  251). 

In  some  cases  of  meningeal  hemorrhage  there  is 
temporary  loss  of  consciousness  from  shock  ;  usually 
the  mind  remains  clear. 

For  purposes  of  diagnosis  it  is  important  to  note  that 
injury  to  the  spine,  direct  or  indirect,  is  the  great  cause 
of  meningeal  hemorrhage.  Very  rarely  it  has  resulted 
from  prolonged  and  severe  muscular  exercise  or  from 
the  rupture  of  an  aneurism  of  the  aorta  into  the  verte- 
bral canal  after  erosion  of  the  vertebrae. 


434         DISEASES   OF  THE   NERVOUS   SYSTEM. 

Meningeal  hemorrhage  may  be  confounded  with 
meningitis,  myelitis,  tetanus,  and  with  hemorrhage  into 
the  cord. 

Meningitis  differs  from  meningeal  hemorrhage  in  that 
the  symptoms  which  are  similar  do  not  come  on  sud- 
denly, and  in  the  presence  of  fever  from  the  commence- 
ment. It  is  important  to  note  that  meningitis  may  be 
secondary  to  meningeal  hemorrhage,  and  that  both  con- 
ditions then  co-exist.  In  tetanus  the  symptoms  are 
never  of  sudden  onset,  and  severe  radiating  pains  do 
not  occur.  On  the  other  hand,  trismus,  an  early  and 
regular  symptom  of  tetanus,  is  absent  in  meningeal  hem- 
orrhage. The  tetanic  spasm  that  occasionally  occurs  in 
newly  born  children  is  due  to  meningeal  hemorrhage 
from  trauma,  and  not  to  true  tetanus. 

Hemorrhage  into  the  Substance  of  the  Spinal  Cord. — 
Hemorrhage  into  the  substance  of  the  spinal  cord  is  rare. 
The  indications  that  point  to  the  occurrence  of  hemor- 
rhage into  the  substance  of  the  spinal  cord  are  the  symp- 
toms of  a  lesion  of  the  spinal  cord,  of  sudden  onset  and 
unaccompanied  by  loss  of  consciousness.  Those  symp- 
toms which  are  of  most  constant  occurrence  are:  (i) 
paraplegia  or  paraplegic  weakness  with  anaesthesia  of 
corresponding  distribution;  (2)  loss  of  control  over  the 
sphincters  ;  (3)  pain  in  the  legs  or  trunk.  The  height 
to  which  the  motor  and  sensory  paralysis  extends  and 
the  precise  character  of  the  loss  of  power  over  the 
sphincters  depend  upon  the  level  of  the  lesion  {vide 
p.  236).  The  condition  of  the  reflexes  is  similarly  varia- 
ble. At  the  onset  or  soon  after  the  onset  of  the  symptoms 
there  may  be  general  convulsions  or  clonic  spasm  of  the 
paralyzed  muscles.  Occasionally  there  is  brief  loss  of 
consciousness  at  the  onset.  After  a  few  days  the  symptoms 
of  myelitis  (secondary)  develop,  and  there  is  a  rise  in 
temperature  and  perhaps  an  extension  of  the  symptoms. 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.         435 

As  with  meningeal  hemorrhage,  the  chief  cause  of 
hemorrhage  into  the  cord  is  injury.  Occasionally  the 
condition  is  preceded  by  exposure  to  cold,  violent  exer- 
tions, or  repeated  coitus,  and  sometimes,  but  rarely,  it 
is  of  spontaneous  occurrence. 

Hemorrhage  into  the  cord  can  hardly  be  confounded 
with  meningeal  hemorrhage.  Both  conditions  have  one 
important  feature  in  common,  /.  e.^  the  sudden  onset  of 
the  symptoms,  but  in  meningeal  hemorrhage  irritative 
symptoms  take  the  lead  and  predominate,  while  in  hem- 
orrhage into  the  cord  the  symptoms  are  essentially  those 
of  a  destructive  and  not  an  irritative  process.  Hemor- 
rhage into  the  cord  may  occur  in  the  course  of  myelitis 
(hemorrhagic  myelitis),  but  in  such  cases,  although  the 
symptoms  of  hemorrhage  are  sudden  in  their  onset,  they 
are  preceded  by  symptoms  that  point  to  myelitis  and  not  to 
hemorrhage.  The  premonitory  symptoms  are  often  slight, 
but  if  they  are  of  longer  duration  than  a  few  minutes 
they  should  be  regarded  as  evidences  of  primary  myelitis, 
to  which  the  hemorrhage  is  secondary.  The  presence 
of  fever  at  the  time  of  the  symptoms  of  hemorrhage  is 
strongly  indicative  of  the  secondary  character  of  the 
hemorrhage.  From  all  other  organic  diseases  of  the 
cord  the  sudden  onset  of  hemorrhage  into  the  cord  is  in 
itself  sufficiently  distinctive. 

Myelitis. — The  clinical  forms  of  myelitis  requiring 
separate  consideration  are  based  upon  (i)  the  mode  of 
onset  of  the  myelitic  process,  and  (2)  upon  the  distribu- 
tion of  the  lesion.  When  the  symptoms  of  myelitis  come 
on  rapidly  and  attain  their  full  development  in  the  course 
of  a  few  days  or  weeks,  the  process  is  acute  j  when  the 
onset  extends  through  a  few  weeks  or  months,  the  pro- 
cess is  subacute  J  and  when  several  months  elapse  in  its 
development,  it  is  spoken  of  as  chronic.     According  to 


43^         DISEASES   OF   THE   NERVOUS   SYSTEM. 

the  distribution  of  the  lesion  the  following  forms  are 
recognized  :  (i)  those  in  which  the  gray  substance  is 
chiefly  or  exclusively  involved — poliomyelitis ;  (2)  those  in 
which  both  gray  and  white  matter  are  involved,  including 
{a)  diffuse  or  general  myelitis^  in  which  a  considerable 
part  of  the  cord  is  diseased  ;  {h)  transverse  myelitis^  in 
which  the  entire  transverse  extent  of  the  cord  is  inflamed  ; 
(<;)  focal  myelitis^  where  the  lesion  is  confined  to  one 
small  area  ;  and  (^)  disseminated  7nyelitis^  in  which  there 
are  many  foci  of  inflammation  scattered  irregularly 
through  the  cord. 

For  clinical  purposes  it  is  convenient  to  recognize  the 
following  forms  of  myelitis  : 

A.  Acute  Myelitis^  including  transverse,  diffuse,  focal, 
and  disseminated  myelitis. 

B.  Chronic  Myelitis. 

C.  Acute  Poliomyelitis  (Infantile  form). 

D.  Subacute  Poliomyelitis  (Form  in  adults). 

Acute  Myelitis. — The  symptoms  that  point  to  the  ex- 
istence of  acute  myelitis  are  rapidly  developed  indica- 
tions of  interference  with  the  chief  functions  of  the 
spinal  cord.  The  degree  and  extent  of  these  symptoms 
vary  much  with  the  degree  and  extent  of  the  myelitis. 
The  following  are  the  phenomena  observed  in  transverse 
myelitis/  which  may  be  taken  as  the  type  of  the  disease  : 

1.  Motor  paralysis,  of  rapid  but  not  sudden  onset, 
below  the  level  of  the  lesion,  partial  or  complete  in  degree. 

2.  Loss  of  sensation,  partial  or  complete,  below  the 
level  of  the  lesion. 

3.  Hypersesthesia  and  girdle  pain  at  the  level  of  the 
lesion. 

'  It  will  be  noted  that  these  are  essentially  the  symptoms  enu- 
merated under  total  transverse  lesions  of  the  sjMnal  cord  {vide  Locali- 
zation). 


THE   DIAGNOSIS    OF   CLINICAL  TYPES.         437 

4.  Loss  of  reflex  at  the  level  of  the  disease  ;  increase 
below  this  level. 

5.  Loss  of  control  over  the  sphincters. 

6.  Trophic  changes  in  the  skin  and  muscles,  varying 
with  the  level  of  the  lesion. 

7.  Vaso-motor  disturbances. 

8.  Changes  in  the  tone  of  the  paralyzed  muscles — 
rigidity,  spasm,  contracture,  or  loss  of  tone,  flaccidity, 
etc.,  according  to  the  level  of  the  lesion. 

According  as  the  lesion  is  in  the  cervical,  dorsal,  or 
lumbar  region  of  the  cord,  the  combination  and  distribu- 
tion of  the  symptoms  enumerated  vary  in  many  important 
respects  (see  Localization,  transverse  lesions).  In  cervical 
myelitis  there  is  paralysis  of  motion  in  the  arms,  legs  and 
trunk,  with  corresponding  sensory  disturbance,  increased 
skin  reflexes  in  trunk  and  legs,  excessive  tendon  re- 
flexes in  lower  extremities,  rigidity  in  the  parts  below  the 
lesion,  retention  of  urine  with  subsequent  incontinence  and 
incontinence  of  faeces.  If  the  lesion  involves  a  considerable 
vertical  extent  of  the  cervical  cord,  there  may  be  consid- 
erable muscular  atrophy  in  the  upper  extremities.  The 
pupils  may  be  contracted  and  there  may  be  optic  neuritis. 

The  symptoms  that  indicate  dorsal  myelitis  are  prac- 
tically those  of  cervical  myelitis,  minus  those  that  relate 
to  the  involvement  of  the  arms,  and  excepting  also  the 
pupillary  changes  and  the  rarer  optic  neuritis. 

The  symptoms  that  point  to  involvement  of  the  lum- 
bar enlargement  are  paraplegia,  loss  of  sensation  in 
the  lower  extremities,  incontinence  of  urine  and  faeces 
from  the  first,  loss  of  reflex  action,  and  atrophy,  with 
RD  and  loss  of  muscle  tonus,  in  the  lower  extremities.' 

^  Atonic  paralysis  of  the  lower  extremities  with  loss  of  control  of 
the  sphincters  and  loss  of  knee-jerks  is  occasionally  observed  in  acute 
myelitis,  not  only  of  the  lumbar  but  also  of  the  cervical  region  of  the 


438        DISEASES   OF  THE  NERVOUS   SYSTEM. 

In  the  majority  of  cases  of  acute  myelitis  the  focal 
symptoms  that  have  been  enumerated  are  preceded  or 
associated  in  their  development  with  constitutional  symp- 
toms, such  as  characterize  most  acute  inflammatory 
processes — malaise,  chilliness,  or  signs  of  prostration, 
and  fever,  slight  or  considerable  in  degree.  The  dis- 
tinctively spinal  symptoms  are  rapid  in  their  onset  and 
reach  a  high  degree  of  severity  in  the  course  of  a  few 
days.  Irritative  symptoms,  such  as  clonic  spasm,  or 
even  general  convulsions  (especially  in  children),  radiat- 
ing pains,  and  pain  in  the  spine,  may  attend  the  onset, 
but  the  evidences  of  irritation  are  soon  displaced  by 
those  of  destruction.  After  the  symptoms  of  the  onset 
have  attained  their  height,  the  distribution  of  the  symp- 
toms may  remain  stationary,  or  there  may  be  an  upward 
or  downward  extension  of  symptoms  of  cord  destruction. 

The  diagnosis  of  the  vertical  extent  of  the  lesion  is 
determined  by  indications  that  are  elsewhere  discussed 
(vide  page  245).  If  the  vertical  extent  is  slight,  the 
case  is  one  of  transverse  myelitis  j  if  it  is  considerable  in 
extent,  it  is  one  of  diffuse  myelitis.  The  recognition  of 
dissetJiinated  foci  of  myelitis  is  often  difficult.  When  pos- 
sible, it  depends  on  symptoms  of  interference  with  the 
functions  of  the  cord  as  a  central  organ,  at  different  levels 
— /.  ^.,  on  the  presence  of  muscular  atrophy  and  RD  or 
loss  of  reflex,  of  such  distribution  as  may  be  caused 
by  foci  at  different  levels  and  cannot  be  explained  by 
the  presence  of  a  single  lesion.  Cases  of  anterior  polio- 
myelitis are  cases  of  focal  myelitis  ;  but  in  addition  to 

cord.  The  symptoms  are  usually  of  rapid  onset  and  soon  change  in 
character,  the  paralysis  becoming  of  the  spastic  type,  the  knee-jerks 
returning  and  growing  excessive,  and  the  sphincteric  control  becoming 
re-established.  The  initial  flaccid  type  of  paralysis  may  be  due  to 
inhibition  from  the  irritative  lesion  in  the  cord  (see  crush  of  spinal 
cord) 


THE   DIAGNOSIS   OF   CLINICAL    TYPES,         439 

this  form  of  focal  myelitis  cases  sometimes  occur  in 
which  there  are  both  sensory  and  motor  symptoms  of 
unilateral  distribution  and  acute  onset,  and  these  belong 
to  the  category  of  acute  myelitis.  When  symptoms  of 
commencing  acute  myelitis  are  followed  by  great  exten- 
sion and  severer  symptoms  of  cord  interference  of  sudden 
onsets  the  exacerbation  is  probably  due  to  hemorrhage 
{hemorrhagic  myelitis). 

The  symptoms  of  subacute  myelitis  are  essentially 
those  of  acute  myelitis,  with  the  difference  that  they 
reach  their  development  more  slowly  and  are  unaccom- 
panied with  such  marked  constitutional  disturbance  at 
the  onset. 

The  etiology  of  acute  myelitis  is  not  sufficiently  dis- 
tinctive to  be  of  much  aid  in  diagnosis.  The  process 
may  follow  exposure  to  cold,  over-exertion,  sexual  excess, 
syphilis,  chronic  alcoholism,  acute  febrile  diseases,  trau- 
matism of  various  kinds,  and  adjacent  inflammatory 
conditions  (as  acute  internal  meningitis,  etc.),  and  rapid 
or  slow  compression. 

When  the  vertical  and  transverse  extent  of  the  lesion 
has  been  determined  by  a  consideration  of  the  distribution 
of  the  motor  and  sensory  paralysis,  the  state  of  reflex 
action  and  the  muscular  irritability,  the  next  question  to 
decide  is  whether  the  process  is  primary  or  whether  it  is 
secondary  to  compression.  This  may  be  done  by  finding 
or  excluding  the  causes  of  compression  of  the  cord, 
especially  bone  disease  {vide  Compression  of  Cord). 

The  diseases  with  which  primary  acute  myelitis  may 
be  confounded  are  hemorrhage  into  the  cord,  polio- 
myelitis, meningitis,  meningeal  hemorrhage,  cauda  equina 
hemorrhage  and  neuritis,  multiple  neuritis,  acute  ascend- 
ing paralysis  and  hysterical  paraplegia. 

The  distinction  of  myelitis  from  hemorrhage  into  the 


440         DISEASES   OF   THE   NERVOUS   SYSTEM. 

cord  is  based  mainly  on  the  sudden  onset  of  the  symp- 
toms in  the  latter  disease  as  contrasted  with  the  rapid 
but  not  sudden  onset  in  the  former.  In  hemorrhagic 
myelitis  the  symptoms  become  suddenly  much  aggra- 
vated, but  the  presence  of  slight  premonitory  symptoms 
as  fever,  numbness,  tingling,  etc.,  lasting  more  than  a  few- 
minutes,  render  the  distinction  from  primary  hemorrhage 
easy.  Speaking  generally,  the  symptoms  of  meningitis  are 
those  of  tissue  irritation  ;  the  symptoms  of  myelitis  are 
those  of  tissue  destruction  in  the  cord.  The  irritative 
symptoms  (pain,  spasm,  rigidity)  that  are  so  prominent 
in  meningitis,  are  absent  in  myelitis,  and  thus  afford  a 
simple  diagnostic  distinction,  but  it  must  not  be  forgotten 
that  myelitis  and  meningitis  often  co-exist,  and  that  in 
these  cases  the  order  and  relative  intensity  of  the  symp- 
toms determines  the  category  to  which  they  belong. 

Myelitis  is  readily  distinguished  from  meningeal  hem- 
orrhage by  the  absence  of  marked  irritative  symptoms 
and  the  gradual  or  more  sudden  development  of  symp- 
toms indicating  a  destructive  cord  lesion.  When  mye- 
litis occurs  in  young  females,  especially  those  of  hysterical 
leanings,  the  affection  may  be  regarded  as  a  hysterical 
paraplegia.  In  lumbar  and  cervical  myelitis  such  a 
mistake  can  scarcely  occur,  but  in  dorsal  myelitis  the 
absence  of  muscular  atrophy  in  the  legs  and  the  presence 
of  increased  knee-jerks  somewhat  favor  the  error.  The 
presence  of  a  girdle  pain,  of  incontinence  of  urine  and 
faeces,  or  of  trophic  changes,  makes  the  presence  of 
organic  disease  exceedingly  probable.  The  presence 
of  ankle  clonus,  as  well  as  increased  knee-jerks,  is  in 
favor  of  organic  disease,  but  does  not  in  itself  settle  the 
question.  If  there  be,  in  addition  to  clonus,  strong  ex- 
tensor spasm  in  the  legs  and  Babinski's  sign,  the  organic 
nature  of  the  disease  is  probable. 


THE  DIAGNOSIS   OF   CLINICAL   TYPES.         44 1 

Three  conditions  allied  clinically  with  acute  myelitis 
remain  to  be  noticed  under  this  head.  They  are  :  (i) 
Abscess  of  the  Spinal  Cord  ;  (2)  Embolism  of  the  Cord  ; 
and  {3)  Caisson  Paralysis. 

Abscess  of  the  Spinal  Cord  is  an  exceedingly  rare  con- 
dition. When  it  occurs  it  is  associated  with  purulent 
spinal  meningitis,  and  the  symptoms  are  those  of  an 
acute  irritative  lesion  of  the  cord  followed  rapidly  by 
those  of  a  destructive  lesion.  When  fully  developed 
the  symptoms  are  essentially  those  of  acute  transverse 
myelitis.  The  distinction  from  myelitis,  when  this  is 
possible,  is  based  on  the  presence  of  a  cause  of  septic 
suppuration,  and  not  on  the  symptoms  themselves.  The 
disease  has  followed  pulmonary  gangrene  and  also  gon- 
orrhoea. It  is  said  also  to  occur  after  severe  injury  to 
the  vertebrae  without  a  wound.  In  most  of  the  cases 
recorded  the  abscess  was  in  the  lumbar  enlargement. 
There  may  be  several  foci  of  suppuration  at  different 
levels  of  the  cord,  and  abscess  of  the  cord  may  coexist 
with  that  of  the  brain. 

Embolism  of  the  Spinal  Cord. — Sudden  paraplegia  occa- 
sionally occurs  in  persons  who  have  organic  heart  dis- 
ease, under  circumstances  that  suggest  that  embolism  of 
the  spinal  cord  may  be  the  cause  of  the  symptoms.  In 
order  to  make  the  diagnosis  of  embolism  of  the  cord 
with  any  degree  of  certainty  in  a  given  case,  it  is  neces- 
sary (i)  that  the  focal  symptoms  should  have  been  of 
sudden  onset  ;  (2)  that  the  patient  should  have  organic 
heart  disease  ;  and  (3)  that  there  should  be  evidence  of 
embolism  elsewhere,  in  the  kidney,  spleen,  or  some  part 
of  the  brain. 

Caisson  Paralysis  ;  Diver  s  Paralysis  j  Paralysis  from 
Lessened  Atmospheric  Pressure. — Men  who  work  at  a  con- 
siderable depth  beneath  the  water,  and  are  exposed  to  an 


442         DISEASES   OF  THE   NERVOUS   SYSTEM. 

atmospheric  pressure  greater  than  twice  that  in  which 
they  ordinarily  live,  are  liable  to  become  suddenly  or 
rapidly  paraplegic  soon  after  coming  back  to  the  sur- 
face, especially  if  such  pressure  is  too  suddenly  reduced. 
The  paralysis  generally  comes  on  within  a  few  hours  after 
the  return  to  the  surface.  There  are  usually  premonitory 
symptoms,  such  as  pains  and  tingling  in  the  legs,  with 
slight  weakness.  Then  the  paralysis  of  the  legs  develops 
rapidly  or  suddenly.  In  severe  cases  the  sphincters  are 
involved,  and  there  is  anaesthesia  of  the  lower  extremities. 
If  the  paralysis  is  partial,  recovery  occurs  in  a  few  days  ; 
if  complete,  the  paralysis  persists  weeks  or  months  with 
partial  or  complete  recovery,  or  it  may  terminate  fatally 
within  a  few  days  or  weeks  of  the  onset.  The  diagnosis 
of  this  condition  presents  no  difficulties  if  its  occurrence 
is  known,  for  its  etiology  is  distinctive.  Symptomati- 
cally  this  form  of  paraplegia  resembles  both  that  from' 
hemorrhage  and  that  from  myelitis.  The  pathological 
condition  which  underlies  it  is  obscure.  In  its  terminal 
stage  the  lesion  resembles  myelitis. 

Chronic  Myelitis. — The  symptoms  of  chronic  myelitis 
vary,  as  do  those  of  acute  myelitis,  with  the  situation  of 
the  myelitic  process.  Motor  paralysis,  sensory  paralysis, 
atrophy  with  RD,  rigidity  and  contracture  may  all  be 
present  in  chronic  myelitis,  but  the  intensely  irritative 
symptoms  of  acute  myelitis,  severe  pain  and  acute 
spasm,  do  not  occur.  In  all  cases  the  development  of 
the  symptoms  is  slow  and  gradual,  and  the  symptoms 
do  not  attain  a  high  degree  of  development  until  many 
months  have  elapsed. 

The  most  common  form  of  chronic  myelitis  is  that 
which  involves  the  dorsal  region.  The  symptoms  in 
such  cases  are  paraplegic  in  distribution.  There  is  loss 
of  power  in  the  legs,  developing  very  gradually,  paraes- 
thesia,  slight   or   considerable   loss  of    sensation  in   the 


THE   DIAGNOSIS   OF  CLINICAL   TYPES.  443 

legs,  increased  knee-jerks  and  later  ankle  clonus  and 
spastic  gait.  There  is  often  some  impairment  of  the 
power  of  the  sphincters.  According  to  the  transverse 
situation  of  the  lesion,  the  symptoms  may  be  quite  sym- 
metrical or  much  more  marked  on  one  side  than  on  the 
other.  When  the  lumbar  or  cervical  enlargement  is 
invaded,  muscular  atrophy  with  RD  is  added  to  the 
other  symptoms.  It  is  most  important  to  remember  that 
chronic  myelitis  is  often  a  "  random  "  process — that  is,  a 
process  which  damages  in  an  irregular  way  the  motor, 
sensory,  reflex,  and  trophic  functions  of  the  spinal  cord, 
without  any  tendency  to  confine  itself  to  structures  that 
subserve  a  particular  function.  The  most  important 
conditions  from  which  chronic  myelitis  has  to  be  dis- 
tinguished, are  slow  compression  of  the  cord  and  primary 
lateral  sclerosis.  In  all  cases  of  slow  compression  of  the 
cord  there  are  nerve-root  symptoms,  at  first  of  an  irrita- 
tive character.  These  symptoms,  which  comprise  pain 
and  acute  spasm,  are  inconspicuous  or  absent  in  chronic 
myelitis. 

Compression  of  the  Spinal  Cord. — Compression  of  the 
spinal  cord  may  be  of  rapid  or  sudden  development,  or 
it  may  be  gradual  in  its  progress.  Rapid  or  sudden 
compression  of  the  cord  is  almost  always  dependent 
upon  injury  which  causes  fracture  or  fracture-disloca- 
tion in  some  part  of  the  spine,  or  which  causes  hemor- 
rhage into  the  membranes  or  cord.  The  symptoms  in 
these  cases  are  the  symptoms  of  a  partial  or  total  trans- 
verse lesion  of  the  cord,  and  the  distribution  of  the 
symptoms,  in  a  given  case,  depends  on  the  level  of  the 
cord  sustaining  the  compression  (z;/^<f  Localization).  The 
cord  is  often  lacerated  as  well  as  compressed  in  cases  of 
fracture-dislocation. 

Slow  compression   of  the   cord  may  be   caused  by  a 


444         DISEASES   OF   THE   NERVOUS   SYSTEM. 

number  of  different  pathological  conditions,  which  are 
separately  considered  elsewhere.  It  is  convenient  to 
indicate  here  the  symptoms  common  to  most  cases  of 
slow  compression,  without  special  reference  to  its  causes. 
Two  classes  of  symptoms  are  observed  in  every  case  of 
slow  compression  of  the  cord  :  (i)  root-symptoms,  and 
(2)  cord-symptoms.  The  root-symptoms  are  those  that 
depend  on  irritation  and  compression  of  nerve-roots  at 
the  level  of  the  compression.  They  include  the  follow- 
ing : 

(a)  Pain,  sharp  and  neuralgic,  in  the  distribution  of 
the  roots  involved.  These  pains  may  occur  in  the 
arms  or  legs,  thorax  or  abdomen,  according  to  the  seat 
of  the  disease. 

(d)  Hypersesthesia  of  the  skin  followed  in  course 
of  time  by  anaesthesia.  The  pains  persist  notwithstand- 
ing the  existence  of  anaesthetic  areas,  and  this  condition 
is  called  ancEsthesia  dolorosa. 

{c)  Muscular  weakness  of  gradual  development,  ac- 
companied with  atrophy  and  RD.  The  distribution  of 
these  symptoms  depends,  of  course,  on  the  level  of  the 
cord  affected. 

To  these  root-symptoms  may  be  added  spasm  in  the 
muscles  that  undergo  wasting,  but  this  is  unusual.  In 
every  case  of  slow  compression,  cord-symptoms  are 
after  a  time  superadded  to  the  root-symptoms.  These 
cord-symptoms  are  the  effects  of  imperfect  conduction 
of  impulses  through  the  cord  itself,  and  include  the  fol- 
lowing : 

(i)  Motor  paralysis  in  the  parts  below  the  level  of 
the  lesion,  usually  of  slow,  sometimes  of  rapid,  devel- 
opment. 

(2)  Increase  of  superficial  and  deep  reflexes  below 
the  lesion. 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.         445 

(3)  Paraesthesise,  numbness,  tingling,  formication, 
sometimes  diminished  sensibility,  and  often  delay  in  the 
conduction  of  painful  stimuli  from  parts  below  the  lesion. 

(4)  Defective  control  of  the  sphincters. 

Both  root-symptoms  and  cord-symptoms  are  commonly 
bilateral  from  the  first,  but  in  cases  where  one  side  of  the 
cord  suffers  before  the  other,  the  symptoms  may  be  for  a 
time  chiefly  or  even  entirely  unilateral. 

The  slow  and  gradual  development  of  the  combination 
of  cord-  and  root-symptoms,  above  enumerated,  justifies 
the  diagnosis  of  slow  compression  of  the  spinal  cord.  The 
presence  of  marked  local  tenderness  of  the  spine  at  a  level 
corresponding  with  the  supposed  seat  of  compression  is 
a  highly  corroborative  symptom.  The  chief  conditions 
that  give  rise  to  such  compression  are  caries  of  the 
spine,  new  growths  of  the  spine,  new  growths  of  the  dura 
or  pia  spinalis,  thickening  of  the  dura  and  compression 
by  an  aneurism  which  has  eroded  the  bones  and  pressed 
on  the  spinal  membranes.  Of  these  various  causes  of 
compression  spinal  caries  is  by  far  the  most  common. 

Crush  of  the  Spinal  Cord. — The  spinal  cord  is  fre- 
quently crushed  in  consequence  of  injury  causing  frac- 
ture-dislocation of  vertebrae  (usually  cervical  vertebrae  or 
lower  dorsal  vertebrae).  The  cases  in  which  this  occurs 
are  of  course  surgical  in  nature,  but  important  questions 
of  a  medical  character  arise  in  connection  with  them, 
which  have  a  direct  bearing  on  prognosis  and  the  ques- 
tion of  operative  treatment. 

The  most  important  thing  to  determine  in  any  case  of 
crush  of  the  cord  is  the  position  and  extent  of  the  injury 
to  the  cord.  The  vertical  level  of  the  injury  and  its 
vertical  extent  may  be  determined  with  the  aid  of  the 
facts  already  presented  in  connection  with  total  trans- 
verse   and    unilateral    lesions  of   the   cord  (see  p.  241). 


44^         DISEASES   OF   THE   NERVOUS   SYSTEM. 

Another  aid  in  the  determination  of  the  level  of  the  lesion 
of  the  cord  is  the  position  of  the  bone  lesion,  as  shown 
by  the  external  evidences  of  damage  to  tfee  vertebrae. 
The  transverse  extent  of  the  injury  to  the  cord  is  much 
more  difficult  to  estimate.  It  is,  however,  very  impor- 
tant that  an  effort  be  made  to  determine  this,  for  on  it 
depends,  in  large  degree,  the  prognosis  of  the  case.  In 
making  this  effort  it  is  essential  to  consider  especially  : 
(i)  the  state  of  motor  power  ;  (2)  the  state  of  sensation  ; 

(3)  the  state  of  the  reflexes  (particularly  the  knee-jerks)  ; 
and,  in  the  case  of  damage  to  the  lower  part  of  the  cord, 

(4)  the  state  of  the  sphincters  of  the  bladder  and  rectum. 
Partial  motor  paralysis  below  the  level  of  the  lesion  indi- 
cates that  the  laceration  of  the  cord  involves  only  part 
of  its  tranverse  extent.*  This  view  would  be  borne  out 
by  the  absence  of  sensory  symptoms  in  the  parts  below 
the  lesion,  or  by  the  slight  degree  of  such  symptoms,  and 
by  the  preservation  or  exaggeration  of  the  knee-jerks, 
if  the  lesion  be  above  the  lumbar  enlargement.  The 
slighter  the  degree  of  motor  or  sensory  loss  below  the 
lesion,  the  slighter  is  the  degree  of  transverse  damage  to 
the  cord.  Complete  motor  paralysis  below  the  level  of 
injury  indicates  that  at  least  a  considerable  transverse 
laceration  of  the  cord  has  occurred.  If  this  complete 
motor  loss  is  associated  with  complete  loss  of  sensa- 
tion below  the  lesion  and  abolition  of  the  knee-jerk,  the 
laceration  of  the  cord  may  be  regarded  as  involving 
practically  the  entire  transverse  extent  of  the  cord.'     If, 

'  Cases  of  this  class  ultimately  make  a  good  recovery  (though  often 
with  considerable  weakness  and  contractures)  in  some  cases.  Some 
of  these  cases  certainly  constitute  the  most  favorable  cases  for, opera- 
tive interference,  but  many  of  the  cases  which  would  do  well  if 
operated  on  would  also  do  well  if  left  alone. 

^  Cases  of  this  type  invariably  terminate  fatally,  whether  operated 
upon  or  not. 


THE  DIAGNOSIS    OF   CLINICAL   TYPES.  447 

however,  the  sensory  loss  is  slight  in  degree,  or  partial 
in  extent,  and  the  knee-jerk  is  not  abolished,  the  lesion, 
though  considerable,  is  not  a  total  transverse  lesion,  and 
the  structures  that  subserve  the  transmission  of  sensi- 
bility are  only  partially  damaged.' 

In  cases  of  crushing  of  the  lumbar  enlargement  of  the 
cord  the  indications  of  the  degree  of  involvement  of 
the  cord  are  the  same  as  stated  above,  except  that  loss 
of  knee-jerk  has  not  necessarily  the  same  sinister  signifi- 
cance as  in  cases  of  injury  above  the  enlargement.  Loss 
of  power  in  the  rectal  sphincter  and  continuous  drib- 
bling of  urine  indicate  extensive  crushing  of  the  lower 
part  of  the  lumbar  enlargement. 

It  is  exceedingly  important  to  distinguish  laceration 
or  crushing  of  the  cord  from  laceration  of  nerve-roots. 
The  distinction  is  not  usually  difficult  if  the  importance 
of  making  it  be  borne  in  mind.  When  the  cord  is  exten- 
sively crushed,  the  nerve-roots  at  the  level  of  injury 
almost  always  suffer  in  some  degree,  but  the  symptoms 
dependent  on  their  damage  are  lost  in  those  of  the  cord 
injury.  When,  however,  the  nerve-roots  suffer  alone  or 
much  more  than  the  cord,'^  the  recognition  of  the  condi- 
tion is  usually  simple.  The  symptoms  referable  to  such 
nerve-root  damage  are  paralysis,  atrophy,  loss  of  reflex, 
and  anaesthesia  in  the  parts  corresponding  to  the  level 
of  the  lesion,  and,  in  cases  where  irritation  is  added  to 

'  Some  ultimate  recovery  of  power  may  occur  in  these  cases.  The 
majority  of  them,  however,  terminate  fatally.  Cases  in  which  there  is 
complete  motor  paralysis  and  persistent  loss  of  knee-jerk  without  con- 
siderable or  complete  loss  of  sensation,  practically  belong  in  the  same 
category  with  the  cases  where  sensation  is  entirely  lost,  for  they  eventu- 
ally terminate  fatally,  though  perhaps  after  a  greater  lapse  of  time. 

-  These  cases  are  much  less  common  than  those  in  which  the  cord 
is  badly  crushed.  They  constitute  a  very  favorable  class  of  cases  for 
operative  interference. 


448         DISEASES   OF   THE   NERVOUS   SYSTEM. 

destruction,  pain,  hypersesthesia,  and  spasm.  These  symp- 
toms are  often  unilateral,  or  much  more  marked  on  one 
side  than  on  the  other.  When  they  are  well  developed, 
they  contrast  strongly  with  the  slightly  developed  par- 
alysis and  anaesthesia  and  well  nourished  muscles  below 
the  level  of  the  lesion. 

The  great  distinguishing  features  of  crushing  of  the 
cord  are  the  inuiiediate  development  of  the  symptoms, 
paralysis,  anaesthesia,  etc.,  after  an  injury  of  the  spine, 
and  the  preponderance  of  symptoms  indicating  a  destruc- 
tive lesion  of  the  cord  over  those  indicating  an  irritative 
lesion.  In  spinal  meningeal  hemorrhage  the  symptoms 
are  of  sudden  onset,  but  the  symptoms  (spasm  and  pain) 
indicating  an  irritative  lesion  greatly  preponderate  over 
those  that  point  to  a  destructive  lesion  (paralysis,  anaes- 
thesia). Cases  of  hemorrhage  into  the  substance  of  the 
cord  (haematomyclia),  of  traumatic  origin,  may  closely 
resemble,  in  the  suddenness  of  their  symptoms  and  the 
preponderance  of  paralytic  phenomena,  cases  of  crush 
of  the  cord.  Indeed,  it  is  doubtful  whether  any  reliable 
points  of  distinction  can  be  given.  This  inability  is, 
however,  not  very  serious,  for  in  most  cases  of  traumatic 
haematomyelia  the  cord  is  in  some  degree  lacerated,  and 
the  prognosis  depends  more  on  the  degree  and  character 
of  the  symptoms  than  on  the  exact  nature  of  the  destruc- 
tive lesion. 

Poliomyelitis. — Poliomyelitis,  inflammation  of  the  ante- 
rior cornua  of  the  spinal  cord,  occurs  as  an  acute  and  as 
a  chronic  or  subacute  process.  Acute  anterior  poliomyelitis 
is  of  much  more  common  occurrence  than  the  chronic 
form,  and  from  its  frequency  and  enduring  effects  is  a 
disease  of  great  importance.  Acute  anterior  poliomy: 
elitis  is  especially  a  disease  of  later  infancy,  but  it  occurs 
at  all  periods  of  life. 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.         449 

Acute  Anterior  Poliomyelitis  (Acute  Atrophic  Paralysis  ; 
Infantile  Paralysis). — In  general  terms  the  symptomatic 
characters  of  acute  anterior  poliomyelitis  are  as  follows : 

(a)  There  is  an  acute  or  rapid,  never  a  sudden,  onset 
of  the  symptoms. 

{h)  The  onset  is  attended  very  generally,  but  not 
always,  with  fever  and  other  constitutional  disturbances. 

(c)  There  is  paralysis  of  rapid  development,  and  often, 
at  first,  of  extensive  distribution.  The  paralysis  soon 
wears  away  except  in  the  region  or  regions  most  affected, 
and  in  these  muscular  atrophy  sets  in. 

(a)  This  muscular  atrophy  advances  rapidly,  and  the 
muscles  involved  are  flaccid  and  present  the  RD. 

The  constitutional  symptoms  attending  the  onset  of 
acute  poliomyelitis  vary  considerably  in  severity  in  differ- 
ent cases.  The  temperature,  which  is  rarely  above  103°, 
is  associated  with  prostration,  headache,  etc.  In  young 
children  there  may  be  delirium,  convulsions,  and  vomit- 
ing ;  in  adults  and  older  children  cerebral  symptoms  are 
rare,  but  sharp  pains  in  the  limbs  are  not  uncommon. 
The  constitutional  symptoms  of  acute  poliomyelitis  are  no 
doubt  due  to  (general)  infection,  the  local  symptoms — 
paralysis,  atrophy,  RD,  and  loss  of  reflex — to  the  de- 
struction of  the  ganglion-cells  of  the  anterior  horns. 

The  paralysis  may  at  first  involve  all  four  extremities, 
but  is  generally  much  less  extensive,  and  may  be  con- 
fined to  part  of  one  limb.  Usually  two  or  three  limbs 
are  affected — both  legs,  both  arms,  a  leg  and  arm,  or  both 
legs  and  an  arm — the  lower  extremities  more  often  than 
the  upper.  When  two  or  more  extremities  are  affected, 
one  usually  suffers  much  more  than  the  others.  The 
cranial  nerves  are  rarely  affected.  In  severe  cases,  in 
which  the  legs  suffer,  the  sphincter  may  be  paralyzed, 
but  this  is  rare. 


450        DISEASES   OF  THE   NERVOUS   SYSTEM. 

After  a  few  days  the  paralysis  lessens  in  range  and 
becomes  confined  to  parts  in  which  the  muscles  rapidly 
waste  and  develop  RD.  After  a  time  permanent  short- 
ening of  the  paralyzed  muscles  occurs,  and  various 
deformities  are  produced.  In  children  the  bones  of  the 
paralyzed  limbs  undergo  an  arrest  of  development,  and 
add  much  to  the  degree  of  the  deformity.  The  leg  suf- 
fers more  often  than  the  arm.  Sometimes  all  the  mus- 
cles of  the  leg  are  paralyzed  and  atrophied  ;  as  a  rule 
the  muscles  below  the  knee  are  7nore  severely  affected  than 
those  above.  The  anterior  tibial  and  peroneal  groups 
suffer  most  often,  as  shown  in  Fig.  49,  and  their  paralysis 
results  in  talipes  equinus — the  most  common  type  of 
deformity  in  poliomyelitis.  Sometimes  the  posterior 
tibial  group  suffers  most,  with  resulting  talipes  calcaneus. 
When  there  is  leg  paralysis  in  poliomyelitis,  the  extensors 
of  the  knee  are  often  affected,  and  their  involvement, 
together  with  interruption  of  the  muscle  reflex  arc  by 
disease  of  the  gray  matter  in  the  cord,  causes  the  loss  of 
the  knee-jerk.  In  the  arm  all  the  muscles  are  never  en- 
tirely paralyzed.  The  thenar  muscles  of  the  hand  and 
the  interossei  are  often  involved.  The  deltoid  also  is 
commonly  paralyzed,  more  often,  indeed,  than  any  of  the 
arm  muscles.  Often  the  extensors  and  flexors  of  the  fore- 
arm are  included  in  the  paralysis  of  the  hand  muscles. 
Both  in  the  arm  and  leg  the  distribution  of  the  paralysis 
is  random ;  occasionally  functionally  related  muscles  only 
are  involved. 

The  recognition  of  acute  poliomyelitis  at  the  time  of 
the  onset  of  the  symptoms  is  by  no  means  always  easy, 
indeed  sometimes  it  is  impossible.  The  symptoms  with 
which  the  disease  is  ushered  in — fever,  prostration,  and 
perhaps  convulsions — are  of  common  occurrence  in  chil- 
dren in  various  general  conditions,  and  are  to  be  regarded 


THE  DIAGNOSIS   OF   CLINICAL  TYPES.         45 1 

as  evidence  of  a  general  process  until  the  distinctive 
nervous  symptom — l(K:alized  paralysis — makes  its  appear- 
ance. In  young  children  it  is  very  easy  to  overlook 
localized  paralysis  in  the  early  stage  of  the  disease,  since 


FIG.  49. 
Poliomyelitis  affecting  the  right  leg  only  (tibial  and  peroneal  type). 

the  prostration  that  accompanies  it  may  cause  partial  and 
temporary  immobility.  Continuous  local  immobility,  as 
of  one  leg  or  one  arm,  cannot,  however,  be  explained  by 
existing  prostration  and  indicates  paralysis.     If  there  is 


452         DISEASES   OF   THE   NERVOUS   SYSTEM. 

paralysis  of  hemiplegic  distribution  (arm  and  leg),  and 
the  onset  is  accompanied  with  decided  cerebral  symp- 
toms (vomiting  and  convalsions),  the  possibility  of  a 
cerebral  palsy  must  be  kept  in  mind. 

After  the  initial  symptoms  have  passed  away,  and  the 
obvious  J^ara/ysis  is  accompanied  with  wasting,  the  diag- 
nosis is  simple.  The  presence  of  RD  in  the  wasted 
and  flaccid  muscles,  the  loss  of  reflexes,  and  the  absence 
of  anaesthesia,  bear  out  the  diagnosis  of  poliomyelitis. 
Yet  while  the  diagnosis  may  usually  be  made  without 
difficulty,  there  are  numerous  conditions  with  which  the 
disease  may  be  at  times  confused.  The  most  important 
of  these  conditions  are  as  follows  :  Infantile  cerebral 
paralysis,  acute  myelitis,  obstetrical  paralysis  (Erb's), 
multiple  neuritis,  hip-joint  disease  and  rickets.  The 
distinction  of  poliomyelitis  from  certain  of  these  con- 
ditions is  elsewhere  considered. 

Subacute  and  Chronic  Poliomyelitis. — It  sometimes  hap- 
pens, especially  in  adults,  that  poliomyelitis  is  subacute, 
instead  of  acute  in  its  onset — the  symptoms  of  paralysis 
not  reaching  their  height  in  the  course  of  a  few  days,  but 
in  the  course  of  one,  two,  or  three  weeks.  These  are 
cases  of  subacute  poliomyelitis.  They  pursue  essen- 
tially the  same  course  as  cases  of  acute  poliomyelitis. 
They  may  terminate  fatally  in  the  stage  of  onset.  The 
cases  must  be  carefully  distinguished  from  cases  of  mul- 
tiple neuritis  and  subacute  myelitis  {vide  p.  509) 

Very  rarely  cases  are  seen  in  which  chronic  muscular 
atrophy  and  paralysis  are  due  to  chronic  inflammatory 
lesions  of  all  the  nervous  structures  of  the  anterior 
horns,  which  are  pathologically  different  from  the  lesions 
of  progressive  muscular  atrophy.  Clinically  these  cases 
of    poliomyelitis    cannot    be    distinguished    from    pro- 


THE  DIAGNOSIS   OF   CLINICAL  TYPES.         453 

gressive  muscular   atrophy  (vide   progressive   muscular 
atrophy). 

Degenerative  Diseases  of  the  Spinal  Cord. — The  de- 
generative diseases  of  the  spinal  cord  may  be  grouped 
as  follows  : 

a.  Primary  and  secondary  spastic  paraplegia — dependent 
on  primary  and  secondary  sclerosis  of  the  lateral  pyra- 
midal tracts. 

b.  Locomotor  ataxia — dependent  on  sclerosis  of  the 
posterior  columns  of  the  cord,  the  posterior  root-zones, 
and  peripheral  sensory  nerves. 

c.  Ataxic  paraplegia — dependent  on  sclerosis  of  both 
posterior  and  lateral  columns. 

d.  Friedreich' s  disease  (hereditary  ataxic  paraplegia,  a 
form  of  ataxic  paraplegia) — in  which  the  lesion  is  a 
combination  of  the  lesions  of  ataxic  paraplegia  with  those 
of  locomotor  ataxia,  developing  in  families  during  the 
adolescent  period. 

e.  Progressive  inuscular  atrophy — in  which  the  lesion  is 
a  slow  degeneration  of  the  ganglion-cells  of  the  anterior 
horns  of  the  spinal  cord  and  anterior  root  fibres  associ- 
ated generally  with  degeneration  of  the  pyramidal  tracts. 

Spastic  Paraplegia. — In  every  case  (except  some 
acute  lesions)  of  transverse  lesion  of  the  spinal  cord 
above  the  level  of  the  lumbar  enlargement  the  paralysis 
of  motion  is  accompanied  after  a  time  wath  well  defined 
symptoms  of  a  spastic  character  below  the  level  of  the 
lesion.  The  symptoms  consist,  first,  of  increased  myota- 
tic  irritability,  as  evidenced  by  increased  knee-jerks  and 
the  presence  of  ankle  clonus,  and,  secondly,  of  tonic- 
spasm  or  rigidity  in  the  paralyzed  extremities.  To  this 
combination  of  symptoms  the  term  "spastic  paraplegia  " 
is  very  appropriately  applied.     The  spastic  phenomena 


454        DISEASES   OF  THE  NERVOUS   SYSTEM. 

depend  on  secondary  degeneration  of  the  pyramidal 
tracts,  and  hence  the  clinical  condition  may  be  denom- 
inated "secondary  spastic  paraplegia." 

The  diseases  of  the  spinal  cord  on  which  secondary 
spastic  paraplegia  may  depend  are  numerous  and  im- 
portant, and  the  degenerative  changes  in  the  pyramidal 
tracts,  on  which  the  spastic  symptoms  depend,  are 
generally  of  secondary  interest  to  the  primary  lesion. 
The  lesions  of  the  cord  that  most  often  cause  spastic 
paraplegia  are  compression  of  the  cord  from  spinal 
caries,  and  acute  and  chronic  myelitis.  Less  frequently 
spastic  paraplegia  results  from  compression  of  the  cord 
from  tumors,  thickening  of  the  dura  mater,  etc.  Sec- 
ondary spastic  paraplegia  may  result  from  other  than 
spinal  cord  lesions.  Thus  it  follows  any  cerebral  condi- 
tion that  causes  bilateral  degeneration  of  the  motor  path, 
as,  for  example,  all  cases  of  bilateral  ordinary  (capsular) 
hemiplegia,  bilateral  meningeal  hemorrhage  in  children, 
general  paralysis  of  the  insane,  etc.  In  some  forms  of 
cerebral  disease  {e.  g.,  some  cases  of  infantile  cerebral 
paralysis),  the  symptoms  due  to  bilateral  secondary  de- 
generation of  the  pyramidal  tracts  are  much  more  ob- 
trusive than  the  evidences  of  the  original  cerebral  lesion, 
and  in  such  cases  the  distinction  from  primary  spastic 
paraplegia  may  be  difficult  or  impossible. 

Primary  Spastic  Paraplegia. — The  term  primary  spas- 
tic paraplegia  is  used  to  designate  cases  in  which  there  is 
a  gradual  development  of  weakness  in  the  lower  extremi- 
ties, with  increase  of  knee-jerks  and  ankle  clonus  and 
tonic  spasm,  often  very  marked,  and  especially  conspicu- 
ous in  the  gait  of  the  patient,  without  any  evidence  of  a 
primary  focal  lesion  in  the  spinal  cord  or  brain.  The 
cases  of  spastic  paraplegia  which  are  due  to  an  unques- 
tionably primary  sclerosis  of  the  lateral  tracts   are  cep 


THE  DIAGNOSIS   OF   CLINICAL  TYPES.         455 

tainly  of  extremely  rare  occurrence.     The  symptoms  in 
such  cases  are  as  follows  : 

1.  Weakness  of  the  lower  extremities  of  exceedingly 
slow  development  (many  months  or  years).  The  weak- 
ness generally  involves  chiefly  the  flexors  of  the  hip,  knee 
and  ankle.  At  first  the  weakness  may  be  greater  in  one 
leg,  but  after  a  time  both  are  equally  affected.  The 
arms  are  rarely  affected,  but  occasionally  they  are  the 
seat  of  some  loss  of  power. 

2.  Rigidity  in  the  m'uscles  of  the  lower  extremities. 
The  spasm  affects  especially  the  extensors.  It  is  least 
when  the  extremities  are  flexed  and  greatest  when 
they  are  extended.  Roughly  speaking  the  spasm  is 
proportioned  to  the  degree  of  paralysis. 

As  a  result  of  the  combined  spasm  and  paralysis  the 
gait  is  peculiar.  The  rigid  leg  is  dragged  forward  as  a 
whole,  the  toes  touching  the  ground,  the  heel  elevated. 
In  children  there  is  often  a  tendency  to  "  cross-legged 
progression  "  from  spasm  of  the  adductors. 

3.  The  knee-jerks  are  exaggerated  and  there  is  ankle 
clonus  and  typical  Babinski's  sign.  The  excess  in 
myotatic  irritability  is  so  great  in  some  instances  that 
there  are  attacks  of  spontaneous  and  violent  clonic  spasm 
in  the  leg  muscles,  such  as  is  produced  by  dorsal  flexion 
of  the  foot.  When  the  ball  of  the  foot  rests  on  the 
ground  there  may  be  excited  similar  clonic  spasm. 

There  is  little  or  no  wasting  of  the  extremities  in  pri- 
mary spastic  paraplegia,  and  sensory  symptoms  are  ab- 
sent. The  sphincters  are  usually  not  affected,  but  they 
may  be  involved  from  the  first. 

As  regards  the  etiology  of  the  disease  there  is  little 
that  is  of  service  in  diagnosis.  The  most  important 
point  in  this  connection  is  that  the  disease  most  often 
begins  between  the  twentieth  and  fortieth  years,  seldom 


456         DISEASES   OF  THE   NERVOUS   SYSTEM. 

later  than  this,  and  not  infrequently  between  the  tenth 
and  twentieth  years. 

In  every  case  in  which  the  slow  onset  of  paralysis, 
spasm,  and  myotatic  increase  suggest  the  existence  of 
primary  spastic  paraplegia,  it  is  very  important  to  exclude 
all  indications  of  a  focal  lesion.  Secondary  spastic  para- 
plegia is  far  more  common  than  the  primary  form,  and 
we  cannot  be  too  careful  in  looking  for  evidences  of 
brain  disease  or  of  spinal  cord  disease,  before  concluding 
that  the  case  is  one  of  primary  spastic  paraplegia.  The 
very  gradual  onset  of  the  symptoms  of  primary  spastic 
paraplegia  is  of  much  importance  in  diagnosis.  We  may 
exclude  at  once  from  this  category  all  cases  in  which 
weakness  and  spasm  are  of  sudden,  acute,  or  subacute 
development.  The  presence  of  very  slight  subjective 
sensory  symptoms — numbness,  tingling,  formication — 
does  not  of  itself  remove  the  case  from  the  category 
of  primary  spastic  paraplegia,  but  the  existence  of  any 
considerable  degree  of  anaesthesia  makes  it  certain  that 
the  lesion  is  not  confined  to  the  lateral  pyramidal  tracts. 

Cases  of  primary  spastic  paraplegia  are  not  rarely  mis- 
taken for  hysterical  paraplegia.  Many  cases  of  primary 
spastic  paraplegia  are  seen  at  the  time  of  life  when  hys- 
terical manifestations  are  common.  In  primary  spastic 
paraplegia  the  rigidity  and  spasm  vary  much  with  the 
position  of  the  limbs — considerable  relaxation  occurring 
on  passive  flexion.  In  hysterical  paraplegia  the  spasm 
does  not  vary  with  the  posture  of  the  limb.  In  primary 
spastic  paraplegia  the  myotatic  excess  is  very  pro- 
nounced ;  in  hysteria  there  may  be  increased  knee-jerks, 
but  pronounced  and  true  ankle  clonus  is  rare,  and  the 
presence  of  such  clonus  should  excite  suspicion  of  organic 
disease.  When  hysterical  sensory  and  mental  phenomena 
are  present,  the  question  of  diagnosis  need  hardly  arise, 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.         45/ 

but  it  must  be  remembered  that  hysterical  symptoms  may 
co-exist  with  this  form  of  organic  disease. 

For  a  time  the  leg  and  arm  of  the  same  side  may  suf- 
fer chiefly,  and  in  such  cases  the  distinction  from  hemi- 
plegia must  be  made.  The  slow  character  of  the  onset, 
absence  of  cerebral  symptoms,  non-involvement  of  the 
face,  and  slight  involvement  of  the  leg  and  arm  of  the 
side  opposite  suffice  to  make  the  diagnosis  clear. 

Locomotor  Ataxia  (Tabes  Dorsalis,  Posterior  Scle- 
rosis).— The  symptoms  of  locomotor  ataxia  depend 
mainly  upon  a  degenerative  process  in  the  sensory 
structures  of  the  central  and  peripheral  nervous  sys- 
tems. The  most  constant  and  significant  alterations 
observed  in  this  disease  are  degeneration  of  the  posterior 
columns  of  the  cord  (especially  the  posterior  median  col- 
umns), the  posterior  root-zones,  and  the  peripheral  neuro- 
muscular (sensory)  segment — structures  that  are  purely 
sensory  in  their  functions.  In  the  brain  the  degenera- 
tions of  locomotor  ataxia  do  not  confine  themselves  so 
strictly  to  -sensory  structures.  Thus  while  degenerative 
changes  occur,  not  rarely,  in  the  optic  nerves  (sensory 
structures),  the  third  and  other  motor  nerves  may  be 
similarly  involved. 

Cases  of  locomotor  ataxia  present  a  great  variety  of 
symptoms.  Of  these  symptoms  some  are  of  such  diag- 
nostic importance  and  are  so  often  observed  that  they 
may  be  looked  upon  as  of  cardinal  importance  ;  others, 
though  often  observed,  or  even  regularly  present  in  ad- 
vanced cases,  are  common  to  so  many  diseases  that  they 
may  be  considered  of  secondary  diagnostic  value. 

The  cardinal  symptoms  of  locomotor  ataxia  are  as 
follows  : 

(i)  Lightning  Pains. — These  are  paroxysmal  pains, 
of  neuralgic  character,  and  often  of  great  severity.  They 


458  DISEASES   OF   THE   NERVOUS   SYSTEM. 

are  felt  chiefly  in  the  legs,  but  may  occur  in   the  trunk, 
arms,  or  head. 

(2)  Ataxia. — The  inco-ordination  of  movement  is 
chiefly  of  the  legs,  but  may  extend  to  the  arms.  It  is 
unassociated  with  any  loss  of  gross  power  or  muscular 
atrophy. 

(3)  Loss  of  Knee-J^erk. 

(4)  The  Argyll -Robei'tson  Symptom. — That  is,  loss  of 
pupillary  reaction  to  light  with  preservation  of  reaction 
during  accommodation.  The  diagnostic  value  of  each  of 
these  symptoms  and  of  certain  combinations  of  them  is 
discussed  later. 

The  order  in  which  the  symptoms  of  locomotor  ataxia 
develop  varies  much  in  different  cases.  Certain  symp- 
toms, however,  usually  develop  early — as  loss  of  knee- 
jerk,  lightning  pains,  Argyll-Robertson  symptom,  and 
optic  atrophy,  when  it  occurs;  while  others,  as  considera- 
ble ataxia,  belong  to  a  later  period,  and  others  still,  as 
loss  of  sphincteric  control,  belong  to  an  advanced  stage. 
A  purely  arbitrary  division  of  the  symptoms  has  been 
made,  having  reference  to  their  most  usual  order  of 
development.  The  convenience  of  this  division  and  its 
general  accuracy,  if  nothing  more,  warrants  its  use.  The 
grouping  is  as  follows  : 

I.  Neuralgic  or  Pre- Ataxic  Stage  of  locomotor  ataxia. 

The  chief  symptoms  of  this  stage  of  locomotor  ataxia 
are  ist,  lightning  pains,  and  2d,  loss  or  diminution  of 
knee-jerk.  There  is  no  alteration  in  the  gait  and  no 
ataxia,  but  there  is  often  inability  to  stand  with  the  feet 
together  and  the  eyes  closed  (Romberg  symptom).*     An- 

'  A  considerable  sway  when  the  eyes  are  closed  and  the  feet  are 
close  together  is  seen  in  many  neurasthenic  and  hysterical  persons, 
but  inability  to  stand  with  the  eyes  closed  is  probably  always  the 
result  of  organic  disease. 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.  459 

Other  symptom  frequently  present  in  this  stage  is  the  loss 
of  light  reflex  of  the  iris  with  preservation  of  reaction 
during  accommodation  (Argyll-Robertson  symptom). 
The  symptoms  of  the  neuralgic  stage,  which  are  of  sec- 
ondary importance  and  inconstant  occurrence,  comprise 
the  following  :  localized  hyperaesthesia  of  the  lower  ex- 
tremities, numbness  and  slight  anaesthesia  of  the  feet, 
diplopia  and  ptosis,  sexual  excitement,  and  amblyopia 
from  optic  nerve  atrophy. 

II.  The  Second  or  Ataxic  Stage. 

The  great  characteristic  of  this  stage,  which  cannot  of 
course  be  sharply  separated  from  the  first,  is  the  presence 
of  distinctly  marked  inco-ordination.  The  gait  is  slightly 
or  considerably  ataxic,  but  the  patient  is  still  able  to  walk, 
at  least  with  help.  Of  course  the  cardinal  and  secondary 
symptoms  of  the  neuralgic  stage  continue  and  become 
more  fully  developed.  In  addition,  severe  paroxysms  of 
pain  in  the  viscera  (crises — laryngeal,  gastric,  vesical) 
may  develop,  there  may  be  loss  of  sexual  power,  and  pe- 
culiar joint  conditions  {vide  page  169)  may  appear.  Loss 
of  control  over  the  sphincters  is  a  feature  of  this  stage. 

III.  The  Third  or  Pseudo- Paralytic  or  Terfninal  Stage. 
— In-  this  stage  the  patient  becomes  unable  "  to  use  his 
legs  "  owing  to  the  high  degree  of  inco-ordination.  On 
account  of  this  and  other  symptoms  he  has  become  prac- 
tically helpless.  The  symptoms  of  the  second  stage  per- 
sist, and  some  of  them  are  more  fully  developed. 

The  separation  of  the  symptoms  of  the  first  and  second 
stages  is  useful  as  emphasizing  the  fact,  which  is  of  con- 
siderable practical  importance,  that  the  development  of 
inco-ordination  is  preceded  by  other  important  sympto?ns. 
While  this  is  generally  true,  it  must  be  noted  that  inco- 
ordination is  sometimes  a  very  early  symptom.  It  may 
indeed  develop  before  the  knee-jerks  are  lost. 


460         DISEASES   OF   THE   NERVOUS   SYSTEM. 

As  in  other  forms  of  organic  disease  the  diagnosis  of 
locomotor  ataxia  should  be  made  so  far  as  possible  on 
objective  grounds.  In  strict  subordination  to  these 
grounds,  the  etiological  facts  of  the  disease  should  be 
allowed  weight.  These  facts  are  that  it  is  essentially  a 
disease  of  middle  and  early  adult  life,  occurs  chiefly  in 
men,  and  is  in  about  ninety  per  cent,  of  the  cases  a  more 
or  less  remote  sequel  (five  to  twenty-five  years)  of 
syphilis. 

The  diagnosis  of  a  fully  developed  typical  case  of 
locomotor  ataxia,  with  its  lightning  pains,  ataxia,  loss 
of  knee-jerks,  altered  sensibility,  and  pupillary  symptoms, 
presents  no  difficulties  even  to  a  novice.  The  problem 
is  by  no  means  so  simple  when  we  have  to  deal  with  the 
early  stage  of  the  disease,  or  when  we  encounter  atypical 
forms.  To  the  consideration  of  such  cases  we  will  now 
pass. 

In  the  early  stage  of  locomotor  ataxia  we  maybe  com- 
pelled to  make  a  diagnosis  in  the  presence  of  a  very  few 
symptoms.  Loss  of  knee-jerk,  combined  with  lightning 
pains  or  Romberg's  symptom,  justifies  a  diagnosis  of 
locomotor  ataxia  in  its  first  stage,  if  we  can  rule  out 
alcoholic  neuritis,  diphtheritic  neuritis,  and  diabetic 
neuritis.  These  same  symptoms  may  occur  in  cases  of 
disease  of  the  anterior  horn  or  anterior  nerve-roots,  but 
the  presence  of  paralysis,  atrophy,  and  RD  would  readily 
exclude  such  cases.  Loss  of  knee-jerk  with  Argyll- 
Robertson  pupils  points  positively  to  locomotor  ataxia. 
The  latter  symptom  may,  however,  depend  on  general 
paralysis,  and  the  combination  with  loss  of  knee-jerk 
might  depend  on  a  complicating  and  not  a  primary  loco- 
motor ataxia.  Mental  and  other  physical  symptoms  are 
usually  sufficiently  marked  in  such  cases  of  general 
paralysis  to  prevent  error. 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.  461 

The  knee-jerk  may  be  present  for  a  time  in  the  early 
stage  of  locomotor  ataxia,  or  it  may  be  merely  diminished 
instead  of  lost,  or  it  may  be  lost  on  one  side  only.  In 
such  cases  a  diagnosis  of  locomotor  ataxia  can  be  justi- 
fied only  by  the  existence  of  typical  ataxia.  If,  in  addi- 
tion to  such  ataxia,  there  are  lightning  pains  or  Argyll- 
Robertson  pupils  the  diagnosis  is  greatly  strengthened. 

When  characteristic  lightning  ^pains  are  the  first 
symptoms  of  locomotor  ataxia  we  can  hardly  do  more 
than  make  a  probable  diagnosis  until  other  symptoms 
appear.  Lightning  pains  associated  with  Argyll-Robert- 
son pupils  constitute  sufficient  evidence  for  a  diagnosis 
of  locomotor  ataxia,  and  lightning  pains  combined  with 
incontinence  of  urine  or  diminished  sexual  power  should 
lead  to  a  decided  suspicion  of  the  disease,  but  do  not 
suffice,  by  themselves,  for  a  positive  diagnosis. 

Locomotor  ataxia  may  be  confounded  with  some 
affections  of  the  peripheral  nerves,  spinal  cord,  and 
brain.  Of  the  peripheral  diseases  with  which  it  may  be 
confounded  two  are  of  especial  importance — alcoholic 
multiple  neuritis  and  diphtheritic  multiple  neuritis  {vide 
pp.  510  and  520.  Of  the  spinal  cord  cases  in  which  con- 
fusion may  arise  the  most  important  is  ataxic  paraplegia 
{vide  p.  438).  No  confusion  should  arise  with  cases  of 
spastic  paraplegia.  In  such  cases  there  are  loss  of 
power,  spasm,  and  increased  knee-jerk,  and  usually 
ankle  clonus.  Actual  loss  of  power  does  not  occur  in 
tabes  until  late  in  the  disease,  when  the  other  character- 
istic symptoms — inco-ordination,  loss  of  knee-jerk,  etc. — 
are  present.  The  spasm  of  spastic  paraplegia  is  never 
seen  in  tabes,  and  the  increased  knee-jerks  and  ankle 
clonus  contrast  sharply  with  the  lost  knee-jerks  of  the 
latter  disease.  In  spastic  paraplegia,  moreover,  there  is 
never  true  ataxia. 


462         DISEASES   OF  THE   NERVOUS   SYSTEM. 

General  paresis  cannot  be  confounded  with  tabes, 
although  the  latter  may  form  a  part  of  the  former. 
Sometimes  (twenty  per  cent,  of  cases)  symptoms  of  spinal 
involvement  (tabes)  develop  first  in  general  paresis, — at 
least  before  the  cerebral  symptoms  become  at  all  marked. 
Loss  of  knee-jerk  in  any  case  of  general  paralysis  in- 
dicates strongly  an  associated  tabes. 

Argyll-Robertson  pupils  are  common  to  both  diseases 
and  do  not  help  in  the  distinction,  and  this  is  true  of  a 
moderate  degree  of  inco-ordination.  Generally  speaking 
the  problem  is  settled  in  favor  of  the  diagnosis  of  general 
paresis  if  the  symptoms  of  dementia  accompany  those  of 
tabes. 

The  inco-ordination  of  locomotor  ataxia  may  be  con- 
founded with  the  ataxia  of  cerebellar  disease,  such  as 
occurs  in  cases  of  cerebellar  tumor.  The  differences  be- 
tween cerebral  ataxia  and  spinal  ataxia  have  been  pointed 
out  {vide  p.  102),  but  sometimes  the  ataxia  of  loco- 
motor ataxia  resembles  closely  that  of  cerebral  tumor. 
Loss  of  knee-jerk  makes  locomotor  ataxia  exceedingly 
probable,  but  it  does  not  settle  the  point,  because  the 
knee-jerk  may  be  temporarily  absent  in  cerebellar  tumor. 
The  presence  of  lightning  pains,  sensory  disorders,  or 
loss  of  light  reflex,  on  the  one  hand,  and  of  cerebral 
symptoms  (optic  neuritis,  headache)  on  the  other,  usu- 
ally enable  the  distinction  to  be  easily  made. 

Ataxic  Paraplegia. — The  symptoms  of  ataxic  para- 
plegia are  essentially  a  combination  of  the  symptoms  of 
locomotor  ataxia  and  those  of  spastic  paraplegia.  This 
peculiar  combination  of  symptoms  is  intelligible  when 
we  consider  that  the  pathological  conditions  which 
underlie  it  present  the  chief  characters  of  the  lesions  of 
the  two  diseases,  locomotor  ataxia  and  spastic  para- 
plegia— that  is  to  say,  there  is  present  in  cases  of  ataxic 
paraplegia  a  degeneration  both  of  the  lateral  pyramidal 


THE  DIAGNOSIS   OF  CLINICAL  TYPES.         463 

tracts  and  of  the  posterior  columns.  But  these  lesions, 
though  bearing  a  close  resemblance  to  those  of  loco- 
motor ataxia  and  ataxic  paraplegia,  are  not  identical 
with  them.  The  most  important  difference  in  the  lesions 
relates  to  those  that  resemble  locomotor  ataxia.  In  the 
first  place  the  degeneration  of  the  posterior  columns  in- 
stead of  being  most  intense,  as  in  locomotor  ataxia,  in 
the  lumbar  region  of  cord,  is  quite  as  well  or  better 
marked  in  the  dorsal  region  of  the  cord.  Secondly,  the 
root-zone  of  the  postero-external  column  of  the  cord  is 
much  less  intensely  sclerosed  than  in  locomotor  ataxia, 
or  it  presents  no  degenerative  changes  whatever.  These 
facts  have  an  important  bearing  in  explanation  of  the 
symptoms  of  ataxic  paraplegia. 

The  essential  and  typical  symptoms  of  ataxic  para- 
plegia are  as  follows  : 

1.  Gradual  Loss  of  Power,  especially  in  the  lower  ex- 
tremities. The  muscles  involved  are  particularly  the 
flexors  of  the  thigh  and  knee,  and  the  effect  of  their 
weakness  is  first  shown  in  walking.  One  leg  may  be 
considerably  more  affected  than  the  other. 

2.  Ataxia,  especially  of  the  lower  e:xtremities,  de- 
veloping gradually  and  pari  passu  with  the  loss  of 
power. 

Gradual  development  of  spasm  in  the  lower  extremi- . 
ties;  together  with 

4.  Increased  knee-jerk,  Babinski's  sign,  and,  usually, 
ankle  clonus. 

Roughly  speaking,  we  may  say  that  a  case  of  ataxic 
paraplegia  presenting  the  typical  symptoms  above 
enumerated  is  clinically  spastic  paraplegia  plus  the 
symptom  ataxia.  Many  cases,  however,  develop  other 
symptoms,  symptoms  which  may  ally  the  case  espe- 
cially with  locomotor  ataxia  on  the  one  hand,  or 
with  spastic  paraplegia  on  the  other.     Of  these  symptoms, 


464        DISEASES   OF   THE   NERVOUS   SYSTEM. 

which  are  virtually  of  secondary  diagnostic  importance 
in  the  majority  of  instances,  the  following  are  the  most 
important  :  {a)  slight  impairment  of  sensation  in  the 
legs  (occasional)  ;  (^)  dull  pain  over  the  sacral  region 
(common)  ;  (c)  girdle  pain  (rare)  ;  (d)  lightning  pains 
(very  rare)  ;  {e)  hypersesthesia  of  lower  extremities 
(rare)  ;  (/)  loss  of  sexual  power  (frequent)  ;  {g)  loss 
of  control  over  sphincters  ;  (/^)  loss  of  light  reflex  ;  (/' ) 
slight  difficulty  in  articulation.  In  very  rare  cases  the 
knee-jerks  may  be  lost,  and  there  may  be  anaesthesia  of 
the  legs.  Such  cases  are  closely  allied  to  locomotor 
ataxia.  As  regards  the  etiology  of  ataxic  paraplegia 
there  is  nothing  sufficiently  distinctive  to  be  of  any 
help  in  diagnosis. 

During  the  early  period  of  ataxic  paraplegia,  when  in- 
co-ordination  is  the  most  obtrusive  symptom,  the  disease 
may  be  mistaken  for  locomotor  ataxia.  The  great  point 
of  distinction  is  the  state  of  the  knee-jerk.  This  is 
lost  in  locomotor  ataxia,  exaggerated  in  ataxic  paraple- 
gia. Occasionally  during  the  early  stage  of  tabes  [vide 
Tabes)  the  knee-jerk  is  retained,  but  in  such  cases  it  is 
never  exaggerated.  The  occurrence  of  extensive  spasm 
in  the  lower  extremities,  such  as  occurs  in  spastic  para- 
plegia, is  also  strongly  in  favor  of  the  existence  of  ataxic 
paraplegia.  Other  points  of  difference  are  the  absence 
in  ataxic  paraplegia  of  marked  sensory  disturbances,  in- 
cluding lightning  pains,  the  absence  of  Argyll-Robertson 
pupils,  etc.  The  diagnosis  is  far  more  difficult  in  the  rare 
cases  that  show  loss  of  knee-jerk  and  considerable  im- 
pairment of  sensation.  Such  cases,  indeed,  resemble 
ataxic  paraplegia  very  closely  in  their  pathological  anat- 
omy. In  ordinary  cases  of  ataxic  paraplegia  the  posterior 
root-zones,  as  above  stated,  are  only  slightly  or  not  at  all 
involved,  and  this  exemption  explains  both  the  absence  of 


THE   DIAGNOSIS    OF   CLINICAL  TYPES.  465 

sensory  symptoms  and  the  retained  knee-jerk.  But  in 
the  cases  under  consideration  this  zone  is  degenerated, 
and  hence  the  loss  of  reflex  and  disturbed  sensation. 
The  diagnosis  from  tabes  would  depend  in  such  a  case 
on  the  presence  of  spasm  and  weakness  in  the  lower 
extremities,  due  to  degeneration  of  the  lateral  pyramidal 
tracts. 

The  distinction  of  ataxic  paraplegia  from  spastic  para- 
plegia is  simple.  It  is  based  on  the  presence  of  inco- 
ordination. When  the  symptoms  of  ataxic  paraplegia 
develop  in  the  course  of  a  few  months — that  is,  have  a 
subacute  onset,  as  they  sometimes  do,  the  distinction  from 
focal  subacute  myelitis,  involving  chiefly  the  posterior 
and  lateral  columns,  may  be  difficult  and  even  impossi- 
ble. The  more  progressive  the  symptoms  the  greater  the 
likelihood  that  the  disease  is  ataxic  paraplegia  ;  if  there 
is  a  retrogressive  tendency  this  is  in  favor  of  focal  mye- 
litis. Some  cases  of  tumor  of  the  middle  lobe  of  the 
cerebellum  cause  both  ataxia  and  weakness  of  the  lower 
extremities — ataxia  from  the  direct  involvement  of  the 
co-ordinating  centre,  weakness  and  spasm  from  pressure 
upon  the  neighboring  pyramidal  tract.  The  presence  of 
headache  suggesting  organic  disease,  of  vomiting,  of 
optic  neuritis,  and  often  of  cranial  nerve  paralysis,  in 
such  cases  makes  the  diagnosis  from  ataxic  paraplegia 
sufficiently  simple. 

Friedreich's  Disease  (Hereditary  Ataxia). — Frie- 
dreich's diseasp  is  a  degenerative  disease  of  the  posterior 
and  lateral  columns  of  the  spinal  cord  which  is  closely 
related  to  ataxic  paraplegia.  In  some  respects  it  also 
bears  a  resemblance  to  locomotor  ataxia.  It  resembles 
ataxic  paraplegia  in  that  there  is  degeneration  of  the 
lateral  pyramidal  tract  of  the  cord,  sometimes  also  of 
the  direct  pyramidal  tract,  and  degeneration  of  the  pos- 


466         DISEASES   OF  THE   NERVOUS   SYSTEM. 

terior  columns.  But  the  degeneration  is  more  intense  in 
the  posterior  column,  especially  in  the  lumbar  region, 
than  is  the  case  in  ataxic  paraplegia.  Moreover,  the  pos- 
terior nerve-roots,  which  escape  degeneration  in  ataxic 
paraplegia,  are  commonly  involved.  In  both  these  re- 
spects the  lesions  of  Friedreich's  disease  resemble  the 
lesions  of  locomotor  ataxia.  Hence  we  may  say  that,  as 
regards  pathological  anatomy,  Friedreich's  disease  is 
intermediate  between  ataxic  paraplegia  and  locomotor 
ataxia,  some  cases  inclining  more  to  the  one  type,  some 
to  the  other. 

In  the  symptoms  of  Friedreich's  disease  this  relation  to 
ataxic  paraplegia  and  to  locomotor  ataxia  is  as  clearly 
shown.     The  principal  symptoms  are  : 

(i)  Ataxia,  first  in  the  legs,  later  in  the  arms.  The 
ataxia  is  shown  first  as  unsteadiness  in  standing  and  walk- 
ing, later  in  a  reeling,  drunken  gait.  Ataxia  is  the  first 
and  most  obtrusive  symptom.  After  a  time  the  head 
often  becomes  the  seat   of  irregular    ataxic  movements. 

(2)  Gradual  loss  of  power  in  the  lower  extremities. 
Generally  there  is  no  considerable  loss  until  late  in  the 
disease,  but  sometimes  it  occurs  early.  It  very  rarely 
amounts  to  complete  paralysis. 

(3)  Loss  of  knee-jerk.  This  is  a  very  early  and  con- 
stant symptom.  In  a  small  percentage  of  cases  the  knee- 
jerk  is  normal,  or  even  exaggerated,  throughout  the  course 
of  the  disease. 

(4)  Speech  disturbance.  This  symptom  does  not  usu- 
ally develop  until  several  years  after  the  development  of 
inco-ordination.  The  character  of  this  speech  defect 
varies  considerably  in  different  cases.  Most  often  there 
is  simple  elision  of  syllables,  or  hesitation,  or  drawling,  or 
the  speech  is  jerky  in  character.  The  defect  may  be 
very  slight. 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.  467 

(5)  Nystagmus.  This  is  a  later  symptom  than  the 
affection  of  speech,  and  of  much  less  frequent  occurrence. 
The  oscillation  usually  does  not  occur  except  when  the 
eyes  are  directed  laterally. 

Beside  these  characteristic  and  important  symptoms 
of  Friedreich's  disease  there  may  be  others  of  less 
diagnostic  significance.  Of  these  the  most  noteworthy 
are  the  following  :  dull  rheumatoid  pains  in  the  legs 
and  back  (not  uncommon),  slight  anaesthesia  of  the  legs, 
lightning  pains  (rare),  loss  of  sexual  power,  fibrillation 
or  jerky  movements  of  the  tongue,  slight  muscular  wast- 
ing (late),  lateral  curvature  of  the  spine,  talipes  equinus, 
contractures  from  muscular  paralysis,  and  vaso-motor 
disturbances. 

There  are  two  etiological  facts  regarding  Friedreich's 
ataxia  that  are  of  much  diagnostic  importance.  The 
first  of  these  is  that  the  disease  is  essentially  a  disease  of 
the  adolescent  period  of  life  and  of  the  years  just  pre- 
ceding puberty.  The  second  is  that  the  disease  has  a 
very  strong  tendency  to  occur  in  several  members  of  the 
same  family,  although  direct  heredity  is  unusual.  But  it 
is  important  to  note  that  isolated  cases  occur. 

Bearing  in  mind  the  facts  of  symptomatology  and  eti- 
ology that  have  been  enumerated,  the  distinction  of 
Friedreich's  ataxia  is  usually  not  difficult.  But  the  diag- 
nosis is  not  always  easy.  Cases  of  ataxic  paraplegia 
occur  (tabetic  form)  that  bear  a  very  close  resemblance 
to  Friedreich's  ataxia.  Friedreich's  ataxia  can  scarcely  be 
confounded  with  the  ordinary  type  of  ataxic  paraplegia, 
because  in  the  former  there  is  regularly  loss  of  knee-jerk, 
in  the  latter  increase  of  knee-jerk  and  ankle  clonus,  and 
because  the  nystagmus  and  defective  articulation  of 
Friedreich's  ataxia  do  not  occur  in  ataxic  paraplegia.  The 
knee-jerk    is,    Irowever,  absent   in    the    tabetic  -  type    of 


468         DISEASES   OF   THE   NERVOUS   SYSTEM. 

ataxic  paraplegia,  and  without  other  points  of  distinction 
to  help  us  the  diagnosis  may  rest  on  the  early  age  of 
development  of  Friedreich's  ataxia,  and  the  occurrence 
of  the  disease  in  several  members  of  a  family.  But 
even  these  criteria  sometimes  fail,  and  it  may  be  im- 
possible to  make  an  absolute  distinction  between  the  two 
diseases. 

The  diagnosis  between  Friedreich's  ataxia  and  locomo- 
tor ataxia  is  never  difficult.  The  important  features  which 
the  diseases  have  in  common  are  the  ataxia  and  the 
loss  of  knee-jerks.  The  early  and  distinctive  sen- 
sory symptoms  of  tabes  (lightning  pains,  etc.),  loss  of 
iris  reflex,  etc.,  separate  a  typical  case  of  tabes  from 
Friedreich's  ataxia.  The  occurrence  of  speech  defects 
and  of  nystagmus  shows  clearly  that  the  case  is  not  one  of 
tabes  but  of  Friedreich's  disease.  The  age  of  onset  also 
becomes  an  important  differential  point.  Friedreich's 
ataxia  always  develops  before  the  twentieth  year,  tabes 
only  very  rarely  before  the  twenty-fifth.  The  family 
occurrence  of  Friedreich's  disease  is  a  most  important 
differential  feature  when  available. 

Friedreich's  ataxia  and  multiple  sclerosis  may  have  in 
common  three  important  symptoms  —  inco-ordination, 
speech  defect,  and  nystagmus.  But  the  inco-ordination 
of  multiple  sclerosis  is  distinctive  in  the  violent  and  wide 
and  jerky  movements  of  the  upper  extremities.  The 
speech  disturbance  of  multiple  sclerosis  is  usually  of  the 
scanning  or  staccato  type  ;  m  Friedreich's  ataxia  there  is 
usually  simple  elision  or  running  together.  The  nystag- 
mus of  multiple  sclerosis  is  constant  and  has  no  reference 
to  voluntary  movements — that  of  Friedreich's  disease  is 
excited  by  lateral  movements.  Besides  these  differences 
in  the  common  symptoms  there  are  the  following  impor- 
tant  differences  :  the  knee-jerks  are  lost  in  Friedreich's 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.  469 

ataxia,  increased  in  multiple  sclerosis  ;  there  is  almost 
always  some  mental  failure  in  multiple  sclerosis,  rarely 
any  in  Friedreich's  ataxia  ;  multiple  sclerosis  occurs  in 
isolated  cases,  Friedreich's  ataxia  almost  always  in  groups 
in  the  same  family. 

Muscular  Atrophies. — Cases  of  disease  are  not  infre- 
quently met  with,  of  which  the  chief  characteristic  is 
slowly  progressive  muscular  wasting,  the  wasting  being 
usually  narrow  in  its  distribution,  at  any  rate  at  first. 
Muscular  wasting  of  limited  extent  (and  rapid  or  slow 
development)  is,  as  we  have  already  seen  {vide  p.  170), 
a  regular  accompaniment  of  various  forms  of  cerebral, 
spinal  cord,  and  peripheral  nerve  disease — that  is,  it  occurs 
in  such  cases  as  one  of  several  equally  important  symp- 
toms. It  is  proposed  to  consider  here  not  that  class  of 
symptomatic  muscular  atrophies,  but  a  class  of  cases  in 
which  slowly  progressive  muscular  wasting  is  the  one 
great  distinctive  feature.  It  must  be  owned  that  the 
pathology  and  even  the  pathological  anatomy  of  some 
of  these  forms  of  muscular  atrophy  is  as  yet  obscure. 
Some  of  the  cases  (progressive  muscular  atrophy)  of 
chronic  muscular  atrophy  are  unquestionably  due  to 
chronic  degenerative  disease  of  the  spinal  cord,  some 
are  probably  due  to  primary  changes  in  the  muscles 
themselves  (muscular  dystrophy),  and  others  still  (pero- 
neal type)  cannot  now  be  safely  classified.  The  forms 
of  muscular  atrophy  that  are  supposed  to  depend  on 
primary  disease  of  the  muscles  (progressive  muscular 
dystrophies)  do  not,  strictly  speaking,  come  within  the 
range  of  this  section,  but  their  clinical  features  are. 
such  as  to  justify  their  consideration  in  connection  with 
the  diseases  of  the  spinal  cord.  The  conditions  to  be 
treated  under  the  head  of  muscular  atrophies  are  as 
follows  : 


470 


DISEASES   OF  THE   NERVOUS   SYSTEM. 


Progressive 
Muscular 
Dystro- 
phies. 


(Due  probably  to 
primary  disease- 
defect  of  the 
muscles.) 


A.  Progressive  Muscular  Atrophy.  (Due 
certainly  to  spinal  cord  disease.) 

B.  The  Peroneal  Form  of  Progressive  Mus- 
cular Atrophy.  (Due  probably  to  spinal 
cord  disease.) 

C.  Pseudo-Hypertrophic' 
Paralysis. 

Z>.  Erb's  Form  of  Pro- 
gressive Muscular 
Dystrophy.  )- 

E.  The  Landouzy-Deje- 
rine  Type  of  Pro- 
gressive Muscular 
Dystrophy. 

Progressive  Muscular  Atrophy  (Chronic  Spinal 
Muscular  Atrophy,  Wasting  Palsy,  Amyotrophic  Lateral 
Sclerosis,  Chronic  Poliomyelitis). — The  distinctive  clin- 
ical feature  of  progressive  muscular  atrophy  is  the  slow 
and  usually  extreme  wasting  of  certain  groups  of  muscles. 
The  pathological  basis  of  the  disease  consists  of  a  grad- 
ual degeneration  of  the  ganglion-cells  of  the  anterior 
horns  of  the  cord,  at  a  level  of  the  cord  corresponding  to 
the  muscles  wasted,  and  of  a  like  degenerative  process  in 
the  anterior  root-fibres  with  which  these  cells  are  con- 
nected. In  association  with  these  lesions  in  the  ganglion- 
cells  and  their  prolongations  the  root-fibres,  there  is 
usually  a  degeneration  of  the  direct  and  crossed  pyra- 
midal tracts  of  the  cord — a  degeneration  which  may  be 
traceable  a  considerable  distance  along  the  motor  path 
in  the  brain. 

Like  the  other  degenerative  diseases  of  the  spinal  cord 
that  have  been  described,  progressive  muscular  atrophy 
fails  to  conform  to  any  rigid  type  in  its  symptoms.     On 


THE   DIAGNOSIS   OF  CLINICAL   TYPES. 


471 


the  otber  hand,  it  resembles  these  diseases  in  having  a 
symptomatology  that  varies  within  considerable  limits. 
Now  in  order  to  comprehend  the  meaning  of  these 
variations  in  type  it  is  essential  to  bear  in  mind  certain 
variations  in  the  lesions  which  will  be  mentioned  in  the 
description  of  the  symptomatology  of  the  disease. 

As  already  stated,  the  striking  clinical  feature  of  pro- 
gressive muscular  atrophy  is  slow  muscular  atrophy.     This 


FIG;  50. 

Atrophy   and  paralysis  with  main  en  griffe  in  chronic   anterior   poliomyelitis. 

(Starrs.) 

muscular  atrophy  commences  in  the  arms  in  about  nine 
tenths  of  all  the  cases  (Aran-Duchenne  type).  In  the 
majority  of  the  cases  beginning  in  the  arm  the  atrophy 
commences  in  the  muscles  of  the  hand,  but  a  considerable 
number  commence  in  the  muscles  of  the  shoulder.  Of 
the  hand  muscles  those  of  the  thenar  and  hypothenar 
eminences  (thumb  and  little  finger)  are  usually  the  first 
to  suffer,  but  the  interossei  and  especially  \.h.Q  first  dorsal 


472        DISEASES   OF  THE  NERVOUS   SYSTEM. 

interosseus  (abductor  indicis)  usually  suffer  very  early. 
This  commencement  of  the  atrophy  in  the  small  muscles 
of  the  hand  and  interossei  is  so  common  as  to  be  a  charac- 
teristic feature  of  the  disease. 

The  atrophy  generally  begins  on  one  side  and  does 


FIG.  51. 

Atrophy  of  the  muscles  about  the  shoulder-blades  and  arms  in  a  case 
of  chronic  anterior  poliomyelitis.     The  triceps  and  latissimus 
dorsi  have  escaped.     (Starrs.) 

not  appear  on  the  other  until  some  time  (often  a  year) 
-has  passed.  When  the  atrophy  commences  in  the  shoul- 
der the  deltoid  generally  suffers  first,  but  whether  hand 
or  shoulder  first  shows  the  wasting  it  soon  extends  to 
other  parts  of  the  limb.  Thus  both  the  flexors  and  ex- 
tensors of  the  wrist,  the  supinators,  the  biceps,  and  triceps 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.         473 

may  In  time  become  one  or  all  involved.  Often  the 
various  muscle  groups  are  unequally  atrophied. 

Usually  after  a  time  the  muscles  of  the  back,  especially 
the  trapezii,  suffer.  A  peculiarity  of  the  trapezius  atrophy 
is  that  its  upper  part  {ultimum  moriens)  often  remains 
intact  when  the  rest  is  much  wasted.  The  sterno-mastoid 
also  is  often  involved.  The  respiratory  muscles  may 
suffer  early  or  late,  and  thus  threaten  life.  Both  inter- 
costals  and  diaphragm  may  be  affected. 

In  exceptional  cases  the  atrophy  commences,  not  in  the 
upper  extremity,  but  in  the  legs.  There  is  good  reason 
to  think  that  the  lesion  that  underlies  these  cases  that 
com?ncnce  in  the  leg  is  of  the  same  nature  as  that  which 
underlies  the  cases  that  begin  in  the  upper  extremity,  but 
as  there  is  no  direct  proof  of  this,  this  class  of  cases  is 
considered  elsewhere  {vide  Peroneal  Type).  Although  it 
is  exceptional  to  meet  with  cases  in  which  the  atrophy 
commences  in  the  leg,  it  is  not  very  unusual  for  cases 
commencing  in  the  arm  to  show  slight  wasting  of  the  legs 
after  a  long  lapse  of  time.  The  face  is  rarely  involved 
in  the  atrophy,  but  the  lips  may  be  wasted  owing  to  the 
not  infrequent  complication  of  progressive  muscular 
atrophy  with  bulbar  paralysis.  The  muscles  that  undergo 
atrophy  gradually  fail  in  power.  This  loss  of  power  is  in 
a  general  way  proportioned  to  the  degree  of  the  wasting^  to 
which  it  is  usually  due.  There  is  an  important  exception 
to  this  general  rule.  It  is  that  the  legs  may  gradually  lose 
power  where  there  is  no  wasting,  or  such  slight  wasting 
that  the  loss  cannot  be  due  to  this.  The  paralysis  that 
accompanies  wasting  depends,  like  the  wasting,  on  dis- 
ease of  the  ganglion-cells  of  the  anterior  horns  ;  the 
paralysis  that  occurs  without  wasting,  or  is  greatly  in  excess 
of  it,  depends  on  degeneration  of  the  pyramidal  tracts  of 
the  cord.     In  addition  to  the  atrophy  and  weakness  that 


474        DISEASES   OF   THE   NERVOUS   SYSTEM. 

occur  in  progressive  muscular  atrophy  there  are  the  fol- 
lowing important  conditions: 

a.  Fibrillary  Contractions  of  the  atrophied  muscles. 
This  is  so  frequent  a  symptom  in  progressive  muscular 
atrophy  as  to  be  characteristic  when  present,  but  it  is 
not  of  invariable  occurrence.  There  is  also  increased 
mechanical  irritability. 

b.  Changed  Electrical  reactions.  When  the  w^asting  is 
slow  there  is  usually  simple  diminution  of  irritability  to 
faradism  and  galvanism.  When  the  wasting  is  rapid  the 
faradic  loss  may  be  out  of  proportion  to  the  galvanic  loss, 
and  there  may  even  be  partial  or  complete  RD  in  certain 
muscles. 

c.  Changes  in  Reflex  Action.  As  a  rule,  there  is  loss  of 
myotatic  irritability  in  the  atrophied  muscles.  The  knee- 
jerk  is  lost  as  soon  as  there  is  even  slight  wasting  of  the 
anterior  thigh  group,  in  those  cases  where  the  leg  is 
affected.  When  the  legs  are  paralyzed  without  wasting 
(that  is,  from  degeneration  of  the  pyramidal  tracts),  the 
knee-jerks  are  exaggerated  and  there  is  clonus.  There 
may,  indeed,  be  true  rigidity,  and  the  leg  symptoms  may 
thus  resemble  closely  those  of  spastic  paraplegia. 

d.  Changes  in  the  Tone  of  the  Muscles.  The  atrophied 
muscles  are  ordinarily  flaccid  and  without  tone  ;  they  are 
in  a  state  of  "  atonic  atrophy."  Occasionally  the  muscles 
are  in  a  state  of  rigidity  from  the  first,  /.  ^.,  they  are  in  a 
state  of  "  tonic  atrophy." 

Beside  the  symptoms  of  progressive  muscular  atrophy 
that  have  been  enumerated  there  may  occur  others  of 
minor  importance.  Thus,  an  early  symptom  is  aching 
pain  in  the  parts  that  become  atrophied,  and  later  there 
may  be  numbness  in  the  parts,  but  there  is  never  any  true 
anaesthesia.  The  unequal  paralysis  of  antagonistic  muscles 
may  lead  to  various  deformities  ;  in  the  hand  the  bird- 


THE  DIAGNOSIS   OF   CLINICAL   TYPES.         475 

claw  hand  {vide  ulnar  paralysis)  is  apt  to  occur.     Sexual 
power  is  frequently  lost.     The  sphincters  are  unaffected. 

Some  of  the  variations  in  the  symptomatology  of  progres- 
sive muscular  atrophy  have  been  briefly  stated  (variations 
in  reflex  state,  m.uscle  tonus,  and  degree  of  wasting).  It 
remains  to  be  indicated  how  these  variations  form  the 
basis  of  certain  clinical  types. 

We  may  regard  as  typical  forms  of  progressive  mus- 
cular atrophy  those  cases  in  which  there  is  considerable 
atrophy  of  the  atonic  sort  in  the  upper  extremity  and  upper 
part  of  the  trunk,  combined  with  weakness  and  rigidity, 
without  atrophy  or  with  very  slight  atrophy^  in  the  legs. 
The  atonic  atrophy  in  the  upper  part  of  the  body 
depends  on  the  degenerative  changes,  already  mentioned, 
in  the  ganglion-cells  of  the  anterior  horns.  The  weakness 
and  spasm  in  the  legs  (with  increased  knee-jerk  and  clo- 
nus )  depend,  on  the  other  hand,  upon  degeneration  of  the 
pyramidal  tract  i^vide  symptoms,  Rigidity  or  Spasm),  and 
on  those  fibres  of  the  tract  that  pass  to  the  leg  centres. 
For,  although  the  pyramidal  tract  may  be  degenerated 
throughout  its  entire  extent,  the  degeneration  of  those 
fibres  that  go  to  the  arm-centres  of  the  cord  does  not 
cause  overaction  in  the  arm  muscles.  This  is  because 
the  ganglion-cells  of  the  anterior  cornua  of  the  cervical 
cord  are  so  extensively  degenerated  that  no  degree  of 
degeneration  of  the  pyramidal  tract  can  cause  the  arm 
muscles  they  innervate  to  overact.  Were  these  ganglion- 
cells  less  degenerated,  or  were  some  of  them  intact  and 
others  degenerated,  the  case  would  be  different.  The 
degenerated  pyramidal  tract  would  in  this  case  cause 
overaction  in  the  cervical  ganglion-cells,  with  resulting 
rigidity  of  the  upper  arm  and  upper  trunk  muscles.  This 
is  precisely  what  happens  in  some  cases— namely,  the 
cases  of  progressive  muscular  atrophy  in  which  there  is 


476        DISEASES   OF   THE   NERVOUS   SYSTEM. 

tonic  atrophy  (often  slight)  in  the  arms,  and  simply 
weakness  and  spasm,  or  spasm  and  weakness  with  mod- 
erate atrophy,  in  the  legs. 

It  is  instructive  to  picture  still  another  pathological 
variation  in  the  same  direction.  Cases  occur  in  which 
the  degeneration  of  the  pyramidal  tracts  forms  the  chief 
lesion,  and  in  which  the  degeneration  of  the  cervical 
ganglion-cells  is  very  slight  indeed.  These  cases  are 
closely  allied  to  a  condition  that  has  been  already  de- 
scribed, viz.,  spastic  paraplegia — in  fact,  they  differ  from 
it  clinically  merely  in  the  slight  atrophy  of  certain  mus- 
cles of  the  upper  extremity. 

Finally,  another  variation,  opposed  in  character  to  the 
last,  must  be  noted.  Cases  occur  in  which  the  ganglion- 
cells  of  the  cervical  and  lumbar  cord  are  all  so  exten- 
sively degenerated  that  notwithstanding  the  presence  of 
degeneration  of  the  pyramidal  tracts,  there  is  no  rigidity 
or  spasm  in  the  lower  extremities.  There  is,  in  such 
cases,  what  may  be  called  universal  atonic  atrophy — the 
arms  and  legs  are  atrophied  (often  extensively),  flaccid, 
and  have  lost  their  myotatic  irritability. 

Enough  has  been  said  to  show  that  in  progressive 
muscular  atrophy  there  are  extensive  variations  in  type, 
based  on  corresponding  variations  in  pathological  anat- 
omy. There  is,  indeed,  every  conceivable  gradation  in 
the  combination  of  spasm,  atrophy,  weakness,  and  myo- 
tatic increase,  between  widespread  tonic  atrophy,  verging 
on  pure  spastic  paraplegia,  on  the  one  hand,  and  on  uni- 
versal atonic  atrophy  on  the  other. 

The  forms  of  progressive  muscular  atrophy  in  which 
spasm  is  marked  have  been  designated  amyotrophic 
lateral  sclerosis,  and  have  been  considered  pathologi- 
cally distinct  from  the  atonic  forms.  This  view  is 
untenable,  since  lateral  sclerosis  is  present,  as  we  have 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.  477 

seen,  even  in  cases  that  present  no  spasm  or  myotatic 
excess;  the  effect  of  the  laterg,!  sclerosis,  in  producing 
overaction  in  the  anterior  cornual  cells,  being  rendered 
inoperative  by  the  degeneration  of  those  cells.  It  is, 
therefore,  more  in  accord  with  the  facts  of  pathology 
to  regard  all  cases  coming  under  the  designation  amy- 
otrophic lateral  sclerosis  as  varieties  of  one  varying 
pathological  state,  than  to  attempt  their  establishment  as 
a  distinct  condition. 

Progressive  muscular  atrophy  has  been  attributed  to  a 
large  variety  of  different  conditions,  but  none  of  these  bear 
a  sufficiently  distinctive  relation  to  the  disease  to  aid  us 
materially  in  diagnosis  [^vide  p.  289).  Two  etiological 
facts,  however,  it  is  well  to  bear  in  mind  :  first,  that  the 
disease  is  essentially  one  of  adult  life,  though  it  may 
commence  in  adolescence  or  in  advanced  life ;  and 
second,  that  when  hereditary  influences  can  be  traced 
they  are  only  rarely  direct. 

The  Peroneal  Form  of  Progressive  Muscular 
Atrophy  (  Leg  Type,  Primary  Neuritic  Atrophy ). — The 
peroneal  form  of  progressive  muscular  atrophy  has  many 
features  that  ally  it  with  the  typical  progressive  muscular 
atrophy  that  has  just  been  described.  It  is,  moreover, 
probable,  upon  the  whole,  that  it  depends  on  changes  in 
the  spinal  cord  similar  to  those  that  cause  the  atrophy 
of  the  typical  form,  though  some  authors  consider  it  a 
peripheral  affection. 

The  feature  of  this  disease  is  slowly  progressive  mus- 
cular atrophy  of  peculiar  distribution.  The  atrophy 
begins  in  the  lower  extremities.  Very  often  the  begin- 
ning is  in  the  extensor  hallucis  longus  or  the  common 
extensor  of  the  toes,  from  which  it  extends  to  the 
peronei  muscles.  The  small  muscles  of  the  foot  may  or 
may  not  be  affected.     The  calf  muscles  atrophy  after  the 


478        DISEASES   OF   THE   NERVOUS   SYSTEM. 

peronei,  and,  last  of  all  and  often  at  a  late  date,  the  thigh 
muscles  are  involved.  After  a  long  time  the  atrophy- 
extends  to  the  small  muscles  of  the  hand.  The  atrophy 
is  always  atonic,  and  usually  symmetrical.  The  knee-jerks 
are  lost  when  the  thigh  muscles  waste— that  is,  late.  The 
electrical  changes  present  the  same  variations  as  in  typical 
progressive  muscular  atrophy.  Fibrillation  occurs  in  the 
wasted  muscles  not  infrequently,  but  not  with  the  con- 
stancy that  it  occurs  in  progressive  muscular  atrophy. 
Vaso-motor  disturbances  are  common,  and  slight  sensory 
disturbance  may  occur.  This  form  of  progressive  mus- 
cular atrophy  is  sometimes  known  as  the  "leg  type,"  to 
distinguish  it  from  the  usual  form,  which  may  be  called 
the  "arm  type." 

The  leg  type  generally  develops  during  early  youth. 
There  may  be  direct  hereditary  influence  and  several 
cases  may  occur  in  the  children  of  the  same  parents. 

The  distinction  between  the  two  described  forms  of 
muscular  atrophy  is  of  course  most  simple  as  a  rule.  As 
the  arm  type  may  involve  the  leg,  and  as  the  leg  type 
may  eventually  involve  the  arm,  an  error  might  occur  if 
we  failed  to  discern  the  order  of  spreading  of  the  atrophy. 
Without  this  knowledge,  a  diagnosis  might  be  difficult ; 
but  the  known  difference  in  the  influence  of  heredity,  and 
the  fact  that  the  arm  type  causes  oiften  unilateral  atrophy 
in  the  leg,  while  the  atrophy  is  symmetrical  in  the  cases 
of  the  leg  type,  might  be  of  service  in  diagnosis.  Both 
types  are  distinguished  from  poliomyelitis  by  their 
gradual  development  and  progressive  course.  The  leg 
type  cannot  be  confused  with  congenital  club-foot  if  due 
care  is  taken  in  bringing  out  the  history  of  the  case.  The 
further  distinction  of  these  types  from  other  conditions 
may  be  conveniently  postponed. 


THE   DIAGNOSIS   OF  CLINICAL  TYPES.         479 

Progressive  Muscular  Dystrophies. — The  progressive 
muscular  dystrophies  are  those  forms  of  muscular  atro- 
phy that  depend,  not  on  disease  of  the  central  nervous 
system,  but  on  primary  lesions  of  the  muscles.  The 
progressive  muscular  dystrophies  have  several  general 
characters  in  common,  which  serve  to  separate  them 
clinically  from  the  typical  form  of  progressive  muscular 
atrophy.  These  characters  are  as  follows  :  (i)  develop- 
ment in  early  youth  ;  (2)  the  occurrence  of  true  or 
false  hypertrophy  of  the  muscles  ;  (3)  the  absence  of 
degenerative  electrical  reactions  ;  (4)  the  absence  of 
fibrillary  contractions. 

The  forms  of  progressive  muscular  dystrophies  to  be 
discussed  are  as  follows  : 

1.  Pseudo-hypertrophic  paralysis. 

2.  Erb's  form  of  progressive  muscular  dystrophy. 

3.  The  Landouzy-Dejerine  type  of  progressive  muscular 
dystrophy. 

Of  these  three  forms,  the  first  may  be  separated  in 
classification  from  the  second  and  third  without  hesita- 
tion. The  second  and  third  forms,  however,  have  so 
many  features  in  common,  that  we  are  scarcely  justified 
in  making  a  sharp  line  between  them.  They  are  here 
considered  separately  for  the  sake  of  convenience. 

Pseudo-Hypertrophic  Paralysis  (Pseudo-Muscular 
Hypertrophy). — The  chief  characters  of  this  disease  are 
as  follows  : 

(a)  Weakness  in  the  muscles  of  the  leg,  and  a  waddling 
gait,  associated  with 

{b)  Apparent  increase  in  the  size  of  certain  leg  muscles, 
especially  the  muscles  of  the  calf,  or  the  calves  and 
thighs.  There  may  be  also  considerable  enlargement  of 
some  of  the  muscles  of  the  shoulder,  especially  the  infra- 


480        DISEASES  OF  THE   NERVOUS   SYSTEM. 


spinati   and   deltoids.     Eventually   many  of  the  hyper- 
trophic muscles  may  undergo  atrophy,  as  shown  in  the 


FIG.  52. 

Pseudo-hypcrtrophic  paralysis. 

muscles  of  the  shoulder  girdle  in  Fig.  52.      In  rare  in- 
stances the  muscles  are  at  no  time  larger  than  normal. 


THE   DIAGNOSIS   OF  CLINICAL   TYPES.         48 1 

U)  A  peculiar  difficulty  in  rising  from  the  ground,  due 
to  weakness  of  the  extensors  of  the  knee  and  hip.  The 
hands  are  placed  upon  the  knees  in  rising,  to  transfer 
part  of  the  weight  of  the  body  from  the  upper  to  the 
lower  part  of  the  femur, — thus  giving  the  extensors  of  the 
knee  a  distinct  mechanical  advantage.  This  and  other 
peculiarities  in  rising  have  justified  the  saying,  "  the 
patient  climbs  up  on  himself."  The  difficulty  is  highly 
characteristic  of  pseudo-hypertrophic  paralysis,  but  is 
not  quite  pathognomonic. 

(d)  After  the  disease  has  lasted  for  a  variable  period 
(several  years),  contractions  occur  in  the  affected  muscles 
(this  contraction  in  the  calf  muscles  causes  talipes 
equinus).     Often  lumbar  lordosis  is  a  late  symptom. 

{e)  The  knee-jerk  is  usually  lost  when  the  extensors 
of  the  knee  are  involved.  The  electrical  reactions  are 
normal,  except  in  a  late  stage  of  the  disease,  when  there 
is  often  diminished  electrical  irritability  to  both  currents. 
There  is  no  disturbance  of  sensibility  and  there  are  no 
fibrillary  contractions. 

(/)  The  disease  is  slowly  progressive. 

(g)  The  disease  is  one  of  early  youth,  and  is  generally 
inherited  through  the  mother,  though  the  mother  may 
not  herself  be  a  subject  of  the  disease. 

Pseudo-hypertrophic  paralysis  is  sometimes  confounded 
with  cases  of  spastic  paraplegia  {v/de  p.  429).  The  two 
conditions  resemble  one  another  in  that  there  are  weak- 
ness in  the  lower  extremities  and  contraction  of  the  calf 
muscles,  in  that  the  calf  muscles  may  be  large  in  each, 
and  in  the  fact  that  both  occur  in  children.  In  spastic 
paraplegia,  however,  there  is  active  contracture  of  the 
calf  muscles,  which  can  be  overcome  by  pressure,  the 
■  gait  is  spastic,  the  knee-jerks  are  increased,  there  is  ankle 
clonus,  and  there  is  no  difficulty  in  rising  from  the  ground. 


482 


DISEASES  OF  THE   NERVOUS   SYSTEM. 


Erb's  Type  of  Progressive  Muscular  Dystrophy 

(so-called  "juvenile  form  "  of  progressive  muscular  dys- 
trophy).— This  is  an  exceed- 
ingly rare  form  of  muscular 
atrophy  possessing  the  follow- 
ing characters: 

(a)  There  is  progressive 
atrophy  and  weakness  in  many 
groups  of  muscles,  especially 
the  muscles  of  the  shoulder, 
the  upper  part  of  the  arm, 
the  pelvic  girdle,  the  thigh, 
and  the  back.  Most  often 
the  atrophy  begins  in  the 
arm.  The  fore-arm  and  leg 
muscles  suffer  very  late,  or  not 
at  all. 

(d)  The  atrophy  of  the  muscle 
fibres  may  or  may  not  be 
associated  with  pseudo-hyper- 
trophy of  some  of  the  muscles — 
usually  there  is  no  pseudo-hy- 
pertrophy. 

(<r)  Fibrillary  contractions  do 
not  occur  in  the  atrophied 
muscles. 

(d)  Galvanic  and  faradic  ir- 
ritability are  reduced  in  the 
affected  muscles  in  proportion 
to  the  degree  of  wasting.  The 
RD  is  never  present  even  in 
slight  degree. 
(<?)  The  disease  usually  affects  several  members  of  the 


FIG.   54. 

Erb's  type  of  progressive  muscular 
dystrophy. 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.  483 

same  family,  and  generally  begins  in  infancy  or  the  ado- 
lescent period  of  life. 

The  Landouzy-Dejerine  Type  of  progressive  muscular 
dystrophy  resembles  Erb's  type  very  closely.  As  in  Erb's 
type,  there  is  widespread,  slowly  progressive  muscular 
atrophy  and  weakness,  fibrillary  contractions  never  occur, 
there  is  diminished  electrical  excitability  of  the  muscles 
but  no  RD,  the  affection  is  one  of  early  life,  and  it 
occurs  usually  in  families. 

The  chief  point  of  difference  between  the  two  types  is 
that  in  the  Landouzy-Dejerine  type  the  muscles  of  the 
face,  shoulder,  and  arms  are  involved  in  the  atrophic 
process,  as  shown  in  Fig.  55.  The  involvement  of  the 
face  muscles  is  such  that  it  gives  to  the  patient  a  pecul- 
iar dull  expression — the  "  myopathic  facies  "  it  is  termed. 
In  consequence  of  the  implication  of  the  orbicularis  oris 
the  lips  are  habitually  separated,  the  lower  lip  is  unduly 
prominent,  and  the  patient  is  unable  to  "pout"  with 
the  lips.  With  the  exception  of  the  involvement  of  the 
face,  the  distribution  of  the  muscular  atrophy  is  much 
the  same  as  in  Erb's. type.  The  atrophy  usually  begins 
in  the  face,  and  in  the  cases  where  it  begins  elsewhere 
the  face  suffers  early.  It  is  said  that  there  is  never  any 
pseudo-hypertrophy  of  muscles  in  cases  of  progressive 
muscular  dystrophy  in  which  the  face  is  involved,  but 
this  is  not  so,  as  shown  in  Fig.  55  (p.  484). 

Both  the  forms  of  progressive  muscular  dystrophy 
that  have  been  thus  briefly  touched  upon  (Erb's  type 
and  the  Landouzy-Dejerine  type)  are  sometimes  observed 
in  members  of  the  same  family,  and  this  is  another 
reason  for  hesitating  to  separate  the  two  types  except 
for  convenience. 

Other  forms  of  progressive  muscular  dystrophy,  based 
on  the  locality  in  which  the  atrophy  commences,  have 


484 


DISEASES   OF   THE   NERVOUS   SYSTEMc 


been  described,  but  when  the  validity  of  these  forms  is 
tested  by  their  association  with  differences  in  etiology, 
there  is  found  to  be  little  reason  for  making  any  further 
separation  into  types — even  for  purely  clinical  purposes. 


FIG.  55. 
Landouzy-D^j^rine  type  of  progressive  muscular  dystrophy. 

Intra-Spinal  Tumor.— Tumors   within   the   spinal 
canal  vary  considerably  as  to  the  symptoms  they  produce. 


THE   DIAGNOSIS   OF  CLINICAL  TYPES.         485 

according  as  they  originate  in  the  cord  on  the  one  hand, 
or  in  the  spinal  membranes  or  the  vertebrae  on  the  other. 
Yet  even  in  the  cases  which  present  the  fewest  cHnical 
features  in  common,  there  is  a  resemblance  sufficiently 
close  to  make  it  desirable  to  consider  both  classes  of 
cases  together. 

The  chief  symptoms  of  intra-spinal  tumor  are  : 

{a)  Pain,  severe  and  constant  at  the  level  of  the  lesion 
and  in  the  parts  below  it.  Usually  the  pain  is  first  felt 
on  one  side  and  extends  after  a  time  to  the  opposite  side. 
The  spine  may  be  locally  tender,  and  there  is  often  a 
distressing  girdle  pain. 

(p)  Paralysis,  of  gradual  onset  and  slow  but  certain 
progression.  The  progress  of  the  paralysis  is  rather 
characteristic  :  one  leg  is  first  involved,  then  the  paralysis 
extends  with  variable  rapidity  to  the  other  leg,  and  the 
patient  eventually  becomes  completely  paraplegic.  In 
some  cases  one  leg  suffers  very  soon  after  the  other,  but 
usually  the  extension  to  the  other  leg  is  not  rapid.  Some- 
times the  tumor  causes  a  rather  rapid  increase  in  the 
paralysis,^  instead  of  the  more  characteristic  gradual 
progression. 

These  two  symptoms,  pain  and  paralysis,  commencing 
on  one  side,  and  extending  to  the  other,  may  be  called 
the  cardinal  symptoms  of  intra-spinal  tumor.  Besides 
these  there  are  other  symptoms  of  considerable  though 
less  diagnostic  importance.  The  chief  of  these  are  rigidity 
of  the  muscles  of  the  spine  and  legs,  contractures 
and  spasmodic  movements  in  the  limbs,  sensory  disturb- 
ances, increased  knee-jerks  and  ankle  clonus  and  increased 
skin-reflexes.  The  exact  distribution  of  the  symptoms 
of  course  varies  with  the  position  of  the  tumor.     The 

^  This  depends  not  on  the  destruction  caused  by  the  tumor  itself, 
but  on  the  myelitis  which  the  growth  causes. 


486        DISEASES   OF   THE   NERVOUS   SYSTEM. 

nature  of  these  variations  may  be  largely  inferred  from 
what  has  been  said  elsewhere  about  unilateral  lesions  and 
total  transverse  lesions  of  the  spinal  cord  (see  p.  241  and 
245).  When  the  lesion  is  above  the  lowest  third  of  the 
lumbar  cord  and  involves  mainly  one  half  of  the  cord  at  its 
level,  the  typical  Brown-Sequard  paralysis  may  be  pro- 
duced (see  p.  241).  Usually  the  lesion  at  no  time  involves 
exactly  one  half  of  the  cord,  and  one  therefore  meets  with 
many  deviations  from  the  typical  Brown-Sequard  paralysis. 
Late  in  the  progress  of  the  disease  a  considerable  part  of 
the  transverse  extent  of  the  cord  is  often  involved,  and 
the  well-known  and  readily  intelligible  symptoms  of  a 
total  transverse  lesion  are  then  more  or  less  closely  repro- 
duced (see  p.  245).  The  nature  of  the  variations  that 
arise,  according  to  the  vertical  position  of  the  tumor 
within  the  spine  (cervical  paraplegia,  dorsal  paraplegia, 
lumbar  paraplegia),  need  not  be  touched  upon  here. 

When  the  presence  of  an  intra-spinal  tumor  seems 
probable,  an  endeavor  must  be  made  to  determine 
whether  the  growth  springs  from  the  cord  or  from  the 
membranes  or  vertebrae.  Very  often  it  is  impossible  to 
determine  this.  When  the  diagnosis  is  possible,  it  is 
based,  not  upon  any  one  peculiarity  of  the  symptoms, 
but  upon  the  consideration  of  a  variety  of  elements  in 
the  case. 

The  conditions  that  point  to  the  existence  of  a  tumor 
of  the  me?nbranes  or  the  bones  are  :  (i)  great  severity  of 
the  root  symptoms  (pain,  spasm)  ;  (2)  the  late  develop- 
ment of  cord  symptoms  (paralysis  and  anaesthesia  below 
lesion)  ;  and  (3)  the  unilateral  distribution  of  cord  symp- 
toms for  some  time  (many  months)  after  cord  symptoms 
first  appear.  On  the  other  hand,  the  conditions  that 
indicate  a  cord  tumor  are  as  follows  :  (i)  the  absence  and 
trifling  character  of  root    symptoms,  such    as  radiating 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.         487 

pains  and  early  spasm  ;  (2)  the  early  development  of 
cord  symptoms  ;  and  (3)  the  rapid  extension  of  cord 
symptoms  from  one  side  to  the  other  (two  weeks  to  several 
months). 

The  diagnosis  of  multiple  tumors  can  be  made  only  by 
the  successive  appearance  of  focal  symptoms  that  differ 
considerably  in  seat,  but  agree  in  character.  The  oppor- 
tunities for  such  a  diagnosis  are  extremely  rare. 

The  diagnosis  of  the  nature  of  the  intra-spinal  mass  is 
almost  always  difficult.  The  causal  indications  some- 
times help  very  much.  The  existence  of  constitutional 
syphilis  or  a  history  of  such  disease  makes  syphiloma 
likely.  A  tubercular  history  makes  solitary  tubercle 
likely.  In  almost  all  cases  of  solitary  tubercle  of  the 
cord  there  is  pulmonary  tuberculosis,  and  in  many  cases 
the  physical  signs  are  unequivocal.  The  presence  of 
multiple  sarcomata  or  neuromata  in  other  parts  of  the 
body  furnishes  an  exceedingly  important  diagnostic 
indication,  but  it  is  only  rarely  available.  A  tumor  of  the 
membranes  may  be  almost  anything  but  glioma  and 
tubercle,  but  is  usually  a  sarcoma.  A  tumor  of  the  cord 
is  probably  a  syphiloma  or  massive  tubercle,  perhaps  a 
glioma. 

The  distinction  between  caries  of  the  spine  with  nervous 
symptoms  and  intra-spinal  tumor  is  sometimes  difficult  at 
first.  The  important  points  in  diagnosis  are  the  follow- 
ing :  in  caries  root-pains  are  rarely  severe,  the  symptoms 
of  compression  of  the  cord  are  bilateral  from  the  first,  or 
become  so  very  soon  after  their  beginning,  and  the  evi- 
dences of  vertebral  disease  (local  tenderness,  irregularity 
of  spines),  are  early  present. 

Sometimes  the  diagnosis  between  chronic  transverse 
myelitis  and  intra-spinal  tumor,  especially  tumor  of  the 
cord,   is  very  difficult.     The   chief   points  of  difference 


488        DISEASES   OF   THE   NERVOUS   SYSTEM. 

are  :  (i)  that  root  symptoms  of  considerable  severity  are 
seldom  absent  in  tumor,  while  they  are  often  absent  or 
slight  in  chronic  myelitis,  in  which  there  is  more  apt  to 
be  a  constant  girdle-pain  ;  and  (2)  that  the  symptoms  of 
tumor  are  usually  actively  progressive,  while  progress  in 
chronic  myelitis  is  generally  slow.  It  is  important  to 
remember  that  considerable  acute  or  subacute  myelitis 
may  be  the  consequence  of  any  tumor  that  compresses 
the  cord,  and  that  an  error  in  diagnosis  may  be  made  if  the 
nature  of  the  original  symptoms  be  not  taken  into  account. 

The  early  nerve-root  pains  of  tumor  should  not  be 
confounded  with  neuralgia.  The  pain  of  neuralgia  is 
rarely  so  constant  and  persistent  as  that  of  intra-spinal 
tumor,  and  seldom  has  the  same  localization  and  radiating 
character. 

Syringomyelia. — Syringomyelia  is  a  condition  of  the 
spinal  cord  characterized  by  the  presence  of  one  or  more 
pathological  cavities  within  the  substance  of  the  cord. 
Such  cavities  may  originate  in  two  ways.  First,  they 
may  depend  on  faulty  closure  of  one  of  the  divisions  of 
the  primary  central  canal  of  the  cord.^  Secondly,  they 
may  depend  on  the  disintegration  of  a  gliomatous  forma- 
tion, which  originates,  usually,  in  embryonal  tissue  about 
the  central  canal.  A  sharp  separation  of  these  two  forms 
of  syringomyelia  is  not  feasible,  since  it  is  probable  that 
in  some  instances  at  least,  the  neurogliar  hyperplasia 
originates  in  superabundant  epiblastic  tissue  left  behind 
during  the  defective  development  of  the  central  canal, 

'  In  the  course  of  development  the  primary  central  canal  of  the  cord 
becomes  divided  into  two  parts,  an  anterior  and  a  posterior.  The 
anterior  division  forms  the  permanent  central  canal .  The  walls  of 
the  posterior  division  gradually  come  together  and  form  the  posterior 
fissure.  The  imperfect  closure  of  either  of  these  divisions  of  the  primary 
central  canal  may  give  rise  to  syringomyelia.  The  word  hydromyelus 
is  sometimes  used  to  designate  a  cavity  of  congenital  origin. 


THE  DIAGNOSIS   OF  CLINICAL  TYPES.         489 

The  cavity  in  syringomyelia  varies  much  in  extent  and 
situation  in  different  cases.  It  encroaches  very  irregularly 
on  the  gray  and  white  substance  of  the  cord,  and  there 
is  consequently  much  variety  in  the  nature  and  dis- 
tribution of  the  symptoms  to  which  the  condition  gives 
rise.  So  indistinctive  are  the  symptoms  of  syringomyelia 
that  it  is  impossible  in  many  instances  to  recognize  the 
condition  during  life.  In  a  certain  number  of  cases, 
however  (probably  a  minority),  there  are  peculiarities  in 
the  symptoms  that  enable  the  diagnosis  of  syringomyelia 
to  be  made  with  a  considerable  degree  of  confidence. 

The  following  are  the  chief  symptoms  of  typical 
syringomyelia  : 

(i)  Slow  muscular  atrophy  resembling  in  its  charac- 
ters that  of  progressive  muscular  atrophy.  This  atrophy 
depends  on  the  involvement  of  the  anterior  horn,  and 
may  be  uni-  or  bilateral,  according  to  the  position  of  the 
cavity  or  the  gliomatous  infiltration  in  which  the  cavity 
formation  is  going  on.  The  atrophy  often  commences 
in  the  arm  muscles,  and  is  apt  to  involve  them  in  much 
the  same  order  as  in  the  Aran-Duchenne  type  of  pro- 
gressive muscular  atrophy  (p.  440).  This  almost  regular 
involvement  of  the  arm  muscles  corresponds  to  the  fact 
that  in  the  cervical  region  the  cord  is  usually  most  ex- 
tensively involved  by  the  lesion.  The  wasted  muscles  are 
the  seat  of  fibrillary  contraction,  and  very  often  present 
the  RD,  especially  in  its  partial  forms  (see  p.  198).  The 
loss  of  power  in  the  wasted  muscles  is  proportional  to  the 
atrophy,  the  wasted  muscles  are  flaccid,  and  the  triceps- 
jerk  is  lost.     In  a  large  majority  of  cases  the  muscles  of 

Sometimes  the  first  intimation  of  the  nature  of  the  case  is  found 
at  autopsy.  In  many  cases  in  which  the  diagnosis  of  syringomyelia 
has  been  made  by  good  observers  the  autopsy  has  failed  to  confinn 
this  diagnosis. 


490        DISEASES   OF  THE   NERVOUS   SYSTEM. 

the  face  and  lower  extremity  are  not  implicated  in  the 
atrophy. 

(2)  Sensory  symptoms  of  peculiar  and  distinctive  char- 
acter. One  of  the  earliest  symptoms  is  a  loss  or  diminu- 
tion of  sensibility  to  temperature  (heat  and  cold),  and 
generally  to  pain,  without  interference  with  the  tactile 
sense.  This  peculiar  partial  or  dissociated  sensory  dis- 
turbance corresponds  in  a  rough  way  to  the  parts  that 
are  the  seat  of  atrophy.  Thus,  if  the  atrophy  affects  the 
upper  extremity,  the  sensory  loss  involves  the  skin  of  this 
part,  and  probably  extends  over  the  shoulder  and  upper 
part  of  the  chest.  The  sensory  loss  is  not  distributed  in 
patches,  but  covers  a  continuous  though  often  irregular 
area.  When  the  atrophy  is  extensive  and  involves  the 
face,  the  latter  may  be  the  seat  of  sensory  disturbances. 
Sometimes  the  peculiar  sensory  loss  involves  one  entire 
lateral  half  of  the  body,  the  mucous  membrane  of  the 
lips,  eyes,  and  anus  being  also  affected.  It  occasionally 
happens  in  advanced  cases  of  syringomyelia  that  also  tac- 
tile sensibility  is  lost.  Pain  in  the  cervico-brachial  region 
may  be  among  the  earliest  symptoms  of  syringomyelia. 

(3)  Trophic  disturbances,  other  than  muscular  atrophy, 
are  often  among  the  earliest  symptoms.  The  vitality  of 
the  atrophied  parts  is  almost  always  lessened,  and  the  loss 
of  sensibility  to  pain  renders  the  skin  of  these  parts 
especially  liable  to  suffer  from  slight  injuries,  which  lead 
to  ulcerations,  eruptions,  etc.  True  trophic  disturbances, 
such  as  overgrowth  of  the  skin  and  nails,  glossy  skin, 
nutritive  alterations  in  the  bones,  whitlows,  etc.,  are  not 
of  rare  occurrence.  CEdema,  and  changes  in  the  tem- 
perature and  color  of  the  affected  limbs  are  very  common. 

Among  the  conditions  of  secondary  diagnostic  impor- 
tance that  are  observed  in  syringomyelia  may  be 
mentioned  scoliosis  of  the  vertebral  column.     The  knee- 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.         49 1 

jerk  is  often  increased  on  the  side  affected,  from  interrup- 
tions of  the  pyramidal  tract.  When  the  lumbar  region  is 
implicated  the  knee-jerk  is  lost.  The  deep  reflexes  of 
the  upper  extremity  are  lost  when  the  disease  is  in  the 
cervical  region.  The  etiology  of  syringomyelia  is  too 
obscure  to  be  of  aid  in  diagnosis.  One  fact,  however, 
regarding  its  occurrence,  it  is  well  to  note.  The  disease 
almost  always  begins  between  the  fifteenth  and  thirtieth 
years  of  life. 

The  peculiar  sensory  disturbances  of  syringomyelia 
serve  to  distinguish  it  from  progressive  muscular  atrophy, 
which  it  may  resemble  very  closely  in  the  character  and 
distribution  of  its  atrophies.  It  is  probable  that  the 
sensory  disturbances  of  syringomyelia  may  be  absent  at 
times  during  the  early  stage  of  the  disease^ — i.e.,  before  the 
neurogliar  hyperplasia  has  begun  to  undergo  the  dis- 
integration that  leads  to  cavity  formation  ;  but  there  is 
excellent  reason  to  believe  that  whenever  there  is  recog- 
nizable muscular  atrophy  in  syringomyelia  there  is  also 
disturbance  of  sensibility.  Hence,  in  cases  of  slow 
muscular  atrophy  in  which  there  arises  the  question  of  a 
diagnosis  between  progressive  muscular  atrophy  and 
syringomyelia,  the  condition  of  sensation  is  to  be  allowed 
great  weight  in  reaching  a  decision. 

The  cavity  formation  in  syringomyelia  may  depend 
not  on  the  breaking  down  of  a  diffuse  gliomatous  infiltra- 
tion, but  on  the  disintegration  of  a  more  or  less  limited 
gliomatous  mass — /.<?.,  a  glioma.  In  such  cases  the  more 
distinctive  symptoms  of  syringomyelia  (local  muscular 
atrophy,  partial  sensory  disturbances,  and  trophic  changes) 
may  be  preceded  by  the  symptoms  of  a  tumor  of  the 
substance  of  the  cord  (see  p.  440). 

The  common  form  or  multiple  neuritis  (alcoholic  form) 
is    sufficiently    distinguished  from  syringomyelia  by   its 


492         DISEASES   OF   THE  NERVOUS   SYSTEM. 

subacute  development,  and  by  the  presence  of  sensory 
loss  of  the  ordinary  type  (tactile  pain  and  temperature 
sense  suffering  about  equally).  Another  form  of  multiple 
neuritis,  namely,  anaesthetic  leprosy,  may  be  confounded 
with  syringomyelia.  The  features  which  the  two  condi- 
tions may  possess  in  common  are  muscular  atrophy  of 
the  Aran-Duchenne  type,  sensory  disturbances,  and 
trophic  changes, — perhaps  including  loss  of  some  of  the 
phalanges.  The  most  important  point  in  the  distinction 
of  the  two  conditions  is  the  fact  that  in  anaesthetic  leprosy 
the  areas  of  anaesthesia  are  small  and  sharply  circum- 
scribed. Usually,  too,  all  forms  of  sensibility  suffer  in 
leprosy  ;  but  too  much  importance  must  not  be  given 
this  fact,  for  cases  occur  in  which  there  is  the  same 
partial  sensory  loss  that  is  so  strongly  suggestive  of  syringo- 
myelia. The  presence  of  the  characteristic  lepra  nodules 
on  some  part  of  the  body  may  determine  the  diagnosis. 

There  is  strong  reason  to  believe  that  the  condition 
known  as  Morvan's  disease  depends  on  syringomyelia. 
The  chief  characteristic  of  Morvan's  disease  is  the  occur- 
rence of  multiple  and  recurrent  whitlows,  accompanied 
with  paresis,  muscular  atrophy,  and  analgesia.  Both 
upper  extremities  are  usually  involved.  It  has  been 
thought  that  the  occurrence  of  whitlows  is  distinctive  of 
Morvan's  disease,  and  that  the  occurrence  of  dissociated 
sensory  symptoms  is  pathognomonic  of  syringomyelia. 
But  it  is  certainly  true  that  whitlows  occur  in  undoubted 
syringomyelia.  It  is  also  true  that  dissociated  anaes- 
thesia was  present  in  some  admittedly  typical  cases  of 
Morvan's  disease.  ^     Probably  the  most  rational  view  of 

'  Dissociated  anaesthesia  (loss  of  pain  and  temperature  sense,  with 
preservation  of  tactile  sense)  has  been  occasionally  observed  in 
hysteria,  hemorrhage  into  the  cord,  locomotor  ataxia,  and  in  com- 
pression of  the  cord  and  nerve-roots.  It  is  therefore  very  far  from 
being  a  pathognomonic  symptom. 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.  493 

the  matter  is  that  what  is  called  Morvan's  disease  is 
merely  syringomyelia  with  preponderating  trophic 
symptoms. 

Diseases  of  the  Peripheral  Nervous  System. 

Neuritis. — The  symptoms  of  neuritis  (or  inflammation 
of  nerves)  are  chiefly  local,  and  vary  in  distribution  with 
the  nerve  or  nerves  affected.  Of  these  local  symptoms 
the  following  are  the  principal : 

(i)  Pain  is  by  far  the  most  obtrusive  symptom  of  neuritis. 
The  nerve  inflamed  is  always  the  seat  of  pain,  which 
may  be  intense,  is  often  burning  or  boring  in  character, 
and  is  increased  by  anything  that  causes  passive  conges- 
tion of  the  part  affected.  Frequently  the  pain  is  not 
confined  to  the  nerve  but  is  present  in  the  parts  to  which 
it  is  distributed. 

(2)  Pressure  upon  the  nerve  at  the  part  inflamed  in- 
creases the  pain. 

Besides  these  symptoms,  which  are  present  in  every 
case  of  neuritis,  there  are  others  which,  though  less 
constant,  are  of  considerable  importance  and  may  be 
of  aid  in  the  diagnosis  of  neuritis.  Thus,  if  the  nerve 
is  accessible,  it  may  often  be  found  to  be  swollen  at 
the  part  inflamed.  Besides  pain  there  may  be  various 
other  sensory  disturbances  ;  numbness,  tingling,  and  hy- 
peraesthesia  are  common  in  the  distribution  of  the  affected 
nerve.  After  some  time  these  symptoms  may  be  followed 
by  anaesthesia,  which  is  not  complete  except  in  small  irregu- 
lar areas.  In  many  cases  of  neuritis  of  motor  or  mixed 
nerves  there  are  decided  motor  symptoms,  including  fibril- 
lary contractions  in  the  affected  muscles,  tremor,  loss  of 
power  (sometimes  complete  paralysis),  and  muscular  atro- 
phy.    The  electrical  reactions  vary  in  different  cases,  ac- 


494        DISEASES   OF   THE   NERVOUS    SYSTEM. 

cording  to  the  severity  of  the  process  and  the  character  of 
the  nerve  involved,  from  no  alteration  whatever  to  com- 
plete RD„  Trophic  and  vaso-motor  symptoms  are  usually 
present.  Especially  common  are  the  changes  in  the 
nutrition  of  the  skin  which  cause  the  condition  known  as 
"glossy  skin."  Eczema,  pemphigoid  and  herpetic  erup- 
tions and  ulcers  are  much  less  common.  The  tempera- 
ture of  the  parts  may  be  changed — at  first  there  may  be 
increase  in  temperature,  later  a  lowering  of  tempera- 
ture may  occur.  Changes  in  the  joints  with  resulting 
limitation  of  movement  are  of  frequent  occurrence. 

In  acute  cases  of  neuritis  there  may  be  some  constitu- 
tional disturbance  at  the  outset.  In  cases  that  are  chronic 
from  the  beginning  such  symptoms  are  absent.  The  pain 
in  chronic  cases  is  less  severe  than  in  acute  cases.  In 
cases  of  slight  neuritis  the  symptoms  may  subside  after  a 
few  weeks,  but  in  most  cases  the  disease  runs  a  much 
longer  course,  and  the  majority  of  acute  cases  pass  into  a 
chronic  stage.  In  some  cases  of  neuritis  the  symptoms 
extend  up  the  limb  affected  ("  neuritis  migrans  "),  and  if 
the  inflammatory  process  ascends  to  the  plexus  from 
which  the  nerve  is  given  off,  all  the  nerves  of  an  ex- 
tremity may  be  affected.  In  some  cases  (especially  cases 
of  so-called  reflex  bladder  paralysis)  the  spinal  cord  or 
its  membranes  become  involved  (myelitis,  meningitis),  and 
through  this  involvement  certain  nerves  of  the  opposite 
side  may  become  the  seat  of  neuritis.  The  variety  of 
neuritis  in  which  several  nerves,  in  symmetrical  parts,  are 
simultaneously  involved  (multiple  neuritis)  will  be  sepa- 
rately considered. 

In  most  cases  in  which  the  symptoms  point  to  the 
existence  of  neuritis  a  cause  for  the  condition  can  be 
found.  Most  often  this  is  injury  of  some  kind  (often 
slight)  ;  sometimes  it  is  adjacent  inflammation  (as  of  a 


THE  DIAGNOSIS   OF   CLINICAL  TYPES.         495 

joint).  Sometimes  the  cause  is  a  preceding  acute  infec- 
tious disease,  or  a  blood  disease,  or  exposure  to  cold,  but 
not  very  rarely  no  adequate  cause  can  be  traced. 

The  distinctive  localization  of  the  symptoms  of  neuri- 
tis to  the  distribution  of  a  particular  nerve  or  combination 
of  nerves,  serves  to  separate  neuritis  from  the  pains  of 
acute  rheumatism.  The  acute  pains  of  some  diseases  of 
the  spinal  cord  (especially  locomotor  ataxia,  myelitis, 
etc.)  may  be  mistaken  for  the  pains  of  neuritis,  but  the 
absence  of  permanent  local  tenderness,  the  irregular  dis- 
tribution of  the  pains,  and  usually  their  paroxysmal 
nature,  will  prevent  an  error.  Moreover,  in  spinal  cord 
disease  evidences  of  the  central  character  of  the  disease 
are  seldom  wanting. 

It  is  exceedingly  important  and  not  always  easy  to  dis- 
tinguish between  certain  cases  of  chronic  neuritis  and 
others  of  neuralgia.  The  considerations  on  which  the 
diagnosis  is  based  are  considered  elsewhere  (Chapter 
VI. — Neuralgia). 

Diseases  of  Special  Nerves. — It  is  convenient  to 
review  the  clinical  forms  of  disease  that  depend  on  mor- 
bid processes  affecting  special  nerves  in  the  anatomical 
order  of  these  nerves,  commencing  with  the  cranial 
nerves.  The  diseases  of  cranial  nerves  that  subserve 
special  forms  of  sensibility  (olfactory,  optic,  auditory) 
have  already  been  sufficiently  considered  elsewhere, 
(Chapters  III.  and  IV.). 

Paralysis  of  the  Ocular  Muscles. 

Paralysis  of  the  Third  Nerve  (Oculo-motorius  Paralysis.) 
— The  special  symptoms  (exclusive  of  symptoms  common 
to  all  ocular  palsies — strabismus,  diplopia,  secondary  de- 
viation) of  paralysis  of  the  whole  of  the  third  nerve  are  : 

(i)  Entire  loss  of  upward  and  inward  movement  of  the 
eye  from  paralysis  of  the  superior  and  internal  rectus  and 


49"        DISEASES   OF  THE  NERVOUS   SYSTEM. 

inferior  oblique  (which  helps  to  elevate  the  eyeball),  and 
partial  loss  ot  downward  movement  from  paralysis  of  the 
inferior  rectus  (the  superior  oblique  being  capable  of 
moving  the  eyeball  slightly  downward  and  outward). 

(2)  Ptosis,  from  paralysis  of  the  levator  palpebrae 
superioris. 

(3)  Loss  of  pupillary  reaction  to  light,  from  paralysis  of 
the  sphincter  iridis, 

(4)  Loss  of  the  power  of  accommodation  from  paralysis 
of  the  ciliary  muscle. 

Usually  all  the  muscles  supplied  by  this  nerve  are 
affected  in  a  peripheral  palsy,  but  they  may  suffer  un- 
equally and  some  may  escape  altogether  ;  not  rarely  the 
levator  and  superior  rectus  are  chiefly  involved,  and 
sometimes  both  escape  together. 

Paralysis  of  the  Fourth  Nerve,  supplying  only  the 
superior  oblique  muscle,  causes  a  partial  loss  of  move- 
ment of  the  eyeball  in  a  downward  and  inward  direction. 
This  defect  in  movement  causes  convergent  strabismus 
when  the  patient  looks  down,  and  diplopia,  which  may  be 
very  troublesome,  when  the  patient  goes  down  stairs. 

Paralysis  of  the  Sixth  Nerve,  supplying  only  the  ex- 
ternal rectus,  gives  rise  to  a  defect  in  the  outward  move- 
ment of  the  eyeball,  with  convergent  strabismus  and 
diplopia  when  the  patient  looks  to  the  side  of  the  para- 
lyzed muscle.  The  head  is  usually  held  inclined  to  the 
side  of  the  paralyzed  rectus. 

Having  established  the  presence  of  paralysis  of  one  or 
more  of  the  motor  ocular  nerves,  it  remains  to  determine 
the  exact  seat  of  the  lesion  and  the  nature  of  the  morbid 
process  causing  the  paralysis.  Paralysis  of  ocular  muscles 
maybe  the  result  of  (i)  disease  of  the  nerves  themselves, 
or  (2)  of  the  fibres  of  origin  between  the  superficial 
origin  and  the   nucleus,  or  (3)  of    the    nuclei   of    the 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.         497 

nerves.  We  have  to  do  here  only  with  disease  of  the 
nerves  themselves,  the  other  conditions  (2  and  3),  and 
the  diagnosis  between  them  and  lesions  of  the  nerve 
trunks  being  considered  elsewhere  (see  Nuclear  Ophthal- 
moplegia). 

If  one  of  the  three  oculo-motor  nerves  (3d,  4th,  or  6th) 
is  paralyzed  alone^  it  is  extremely  probable  that  the  lesion 
causing  it  is  at  the  base  of  the  brain.  In  the  case  of 
the  third  nerve,  the  nerves  of  both  sides  may  be  affected 
and  the  lesion  nevertheless  be  a  basal  lesion,  for  these 
nerves  lie  very  close  together  in  the  space  between  the 
peduncles  {vide  Fig.  13). 

But  in  the  case  of  the  fourth  and  sixth  nerves,  which 
are  widely  separated  at  their  superficial  origins  and  from 
their  mates  of  the  opposite  side,  the  involvement  of  the 
nerves  of  opposite  sides  almost  always  excludes  a  lesion 
of  the  trunk.  The  sixth  nerve  has  a  long  course  between 
its  superficial  origin  and  its  passage  through  the  sphenoidal 
fissure,  and  therefore  suffers  more  frequently  than  any 
other  ocular  nerve.  As  it  passes  near  the  fifth  nerve  in 
its  course  over  the  pons,  these  two  nerves  may  suffer 
together,  and  this  combination  points  certainly  to  a 
basal  lesion.  Paralysis  of  the  sixth,  seventh,  and  eighth 
also  indicates  a  basal  lesion,  but  paralysis  of  the  sixth 
with  the  seventh  and  without  the  eighth,  shows  that  the 
lesion  is  not  at  the  base,  but  within  the  pons.  If  all  of 
the  motor  ocular  nerves  of  one  eye  are  involved,  the 
disease  is  certainly  at  or  near  the  sphenoidal  fissure. 
These  indications  will  serve,  in  most  instances,  to  locate 
the  position  of  the  morbid  process. 

Various  morbid  processes  cause  paralysis  of  the  oculo- 
motor nerves.  Probably  the  most  frequent  causes  are 
syphilitic  new  growths  and  chronic  syphilitic  meningitis 
at  the  base  of  the  brain.     When  the  nerves  are  damaged 


49^         DISEASES   OF  THE   NERVOUS   SYSTEM. 

in  the  orbit  it  is  usually  as  the  result  of  cold  (so-called 
"  rheumatic  "  neuritis),  or  of  cellulitis,  or  of  an  orbital 
growth.  When  third-nerve  paralysis  depends  on  "  rheu- 
matic neuritis  "  the  paralysis  is  always  one-sided,  and 
usually  only  one  nerve  is  involved,  or  a  single  branch  of 
a  nerve,  or  two  or  more  adjacent  branches.  The  onset  of 
such  cases  is  generally  attended  with  pain  about  the  orbit. 
Bilateral  partial  ophthalmoplegia  probably  sometimes 
depends  on  alcoholic  neuritis.  Occasionally  diphtheria 
is  followed  by  paralysis  (usually  partial)  of  the  external 
(as  well  as  the  ciliary  muscle)  muscles  of  the  eyeball. 
Usually  the  internal  recti  suffer  most  (or  alone),  but  all 
the  muscles  may  be  involved.  Similar  paralysis  may 
follow  influenza. 

The  ocular  paralysis  that  so  frequently  accompanies 
locomotor  ataxia  is  usually  of  central  (nuclear)  origin, 
and  it  is  uncertain  whether  it  is  ever  the  result  of  periph- 
eral disease.  The  decision  as  to  the  nature  of  the  lesion 
(new  growth,  aneurism,  gumma,  chronic  syphilitic  menin- 
gitis, etc.),  in  a  given  case  of  ocular  paralysis  from  dis- 
ease within  the  cranium,  will  depend  on  the  application 
of  principles  that  have  been  already  stated  (see  Diagnosis 
of  the  Nature  of  the  Lesion  ;  also  Intracranial  Tumor, 
Meningitis,  and  Aneurism).  Not  rarely  it  is  impossible  to 
determine  with  certainty  the  nature  of  the  lesion. 

Paralysis  of  the  Fifth  Nerve. — The  symptoms  of 
paralysis  of  the  fifth  nerve  vary  according  as  they  result 
from  disease  of  the  sensory  or  motor  root  or  from  disease 
affecting  both  roots. 

The  chief  symptoms  of  disease  of  the  sensory  division 
are  : 

I.  Loss  of  sensibility  in  the  parts  supplied  by  the  fifth 
nerve.  This  loss  of  sensibility  may  involve  the  entire 
region  supplied  by  the  fifth  when  there  is  disease  of  the 


THE  DIAGNOSIS   OF   CLINICAL  TYPES.         499 

root  of  the  nerve,  or  when  all  three  branches  (first,  sec- 
ond, and  third)  are  involved  by  a  lesion  at  the  base  of  the 
brain.  When  individual  branches  are  involved  the  anaes- 
thesia is  limited  to  the  regions  supplied  by  them.  There 
is  also  loss  of  sensibility  in  the  mucous  membranes  sup- 
plied by  the  nerve  (nose,  tongue,  and  mouth  on  the  side 
of  the  lesion).  In  some  cases  the  back  of  the  tongue  and 
the  soft  and  hard  palate  share  in  the  sensory  loss,  but  in 
others  (even  where  the  entire  nerve  is  probably  involved) 
only  the  anterior  two  thirds  of  the  tongue  is  insensitive. 

II.  Pain,  often  sharp  and  burning,  may  precede  the 
development  of  anaesthesia. 

III.  Loss  of  taste.  Loss  of  taste  on  one  side  of  the 
tongue  and  palate  results  from  severe  disease  of  the  sen- 
sory portion  of  the  fifth.  When  taste  is  not  involved  in 
lesions  of  the  fifth  it  is  probably  because  the  disease  is 
partial  or  the  lesion  is  within  the  pons.  Loss  of  taste 
confined  to  the  anterior  two  thirds  of  the  tongue  occurs 
where  the  lingual  branch  of  the  fifth  is  diseased  between 
the  peripheral  distribution  and  its  junction  with  the  chorda 
tympani  (Fig.  54). 

IV.  Trophic  changes.  The  chief  trophic  alterations 
that  occur  in  consequence  of  disease  of  the  sensory  por- 
tion of  the  fifth  nerve  are  those  of  the  eye.  The  cornea 
becomes  dry  and  opacities  appear  ;  ulceration  occurs,  and 
this  may  go  on  to  perforation  and  eventual  destruction  of 
the  globe  of  the  eye.  These  ocular  changes  are  especially 
frequent  in  irritative  disease  involving  the  Gasserian  gan- 
glion or  the  nerve  anterior  to  it,  and  are  rare  in  lesions  be- 
tween the  ganglion  and  the  superficial  origin  of  the  nerve 
from  the  pons.  Another  trophic  change  that  results 
especially  from  lesions  that  affect  the  Gasserian  ganglion 
or  the  nerve  anterior  to  it  is  herpes  zoster,which  most  often 
affects  the  superior  maxillary  distribution  of  the  nerve. 


500        DISEASES   OF  THE   NERVOUS   SYSTEM. 

The  principal  symptoms  of  disease  of  the  motor  portion 
of  the  nerve  are  weakness  of  the  masseter,  temporal,  and 
external  pterygoid  muscles  on  the  side  of  the  lesion. 
The  weakness  of  the  masseter  and  temporal  muscles  is 
evident  when  the  finger  is  placed  over  these  muscles 
and  the  patient  brings  the  upper  and  lower  teeth  forcibly 
in  contact. 

The  pterygoid  paralysis  is  shown  by  defective  lateral 
movement  of  the  lower  jaw,  which  can  be  moved  towards 
but  not  away  from  the  side  of  the  paralyzed  muscle.  In 
the  course  of  a  few  weeks  the  paralyzed  muscles  atrophy 
and  the  temporal  and  zygomatic  fossae  show  this  by 
growing  sunken. 

The  tensors  of  the  palate  and  tympanum  are  supposed 
to  be  paralyzed  by  a  lesion  of  the  fifth,  but  no  clinical 
evidence  of  it  can  be  detected. 

It  is  probably  correct  to  attribute  to  disease  of  the 
descending  root  (see  p.  49)  of  the  fifth  the  peculiar  and 
rare  condition  known  as  facial  hemiatrophy,  in  which 
there  is  a  gradual  and  considerable  wasting  of  one  side 
of  the  face,  the  bones  and  subcutaneous  tissues  being  the 
chief  seat  of  the  wasting. 

Complete  paralysis  of  the  fifth  nerve,  including  paraly- 
sis of  the  motor  portion  of  the  nerve,  can  hardly  be  con- 
founded with  any  other  condition.  When,  however,  the 
sensory  portion  is  alone  affected  and  there  is  anaesthesia 
of  adjacent  areas,  difficulties  in  diagnosis  may  arise. 

In  hemianaesthesia  the  loss  of  sensibility  includes  the 
very  parts  supplied  by  the  sensory  portion  of  the  fifth. 
But  in  hemianaesthesia  the  loss  involves  also  the  back  of 
the  head,  the  limbs  and  the  trunk  on  one  side,  and  often 
there  is  hemianopsia.  When  pain  is  the  only  symptom  of 
disease  of  the  fifth,  as  it  may  be  for  a  time,  it  is  impor- 


THE  DIAGNOSIS   OF  CLINICAL  TYPES.  50I 

tant  to  avoid  confounding  the  condition  with  neuralgia, 
which  it  may  closely  resemble  (see  Neuralgia). 

The  diagnosis  of  the  position  of  the  disease  that  gives 
rise  to  paralysis  of  the  fifth  is  based  mainly  on  the 
extent  of  the  anaesthesia  and  the  conditions  associated 
with  the  paralysis. 

Paralysis  of  all  three  divisions  of  the  sensory  portion, 
with  paralysis  of  the  motor  portion  of  the  nerve,  points  to 
disease  at  the  base  of  the  brain  or  possibly  at  the  Gas- 
serian  ganglion.  If  there  is  also  paralysis  of  the  sixth 
nerve  the  lesion  is  surely  near  the  point  of  emergence  of 
the  fifth  at  the  side  of  the  pons.  If  the  loss  of  function  is 
confined  to  the  distribution  of  the  superior  maxillary  div- 
ision of  the  nerve,  the  lesion  is  probably  at  the  sphenoi- 
dal fissure  or  in  the  orbit,  and  this  belief  is  strengthened  if 
there  is  also  paralysis  of  the  nerves  to  the  eyeball.  If  the 
inferior  maxillary  division  of  the  nerve  is  alone  affected 
the  lesion  is  probably  in  the  spheno-maxillary  fissure 
or  in  the  superior  maxillary  bone.  Paralysis  of  the  sec- 
ond and  third  divisions  of  the  nerve,  without  involvement 
of  t"he  first  division,  is  generally  due  to  disease  in  or  near 
the  spheno-maxillary  fossa. 

Crossed  paralysis  of  the  fifth  nerve  (fifth  on  one  side, 
arm  and  leg  on  the  other)  depends  usually  on  a  lesion 
within  the  pons.  The  association  of  conjugate  deviation 
(to  the  side  of  the  lesion)  with  paralysis  of  the  fifth  is 
positive  evidence  of  a  pontine  lesion, 

A  knowledge  of  the  locality  of  the  lesion  aids  us  in 
determining  its  nature.  Thus,  a  pontine  lesion  causing 
fifth  nerve  paralysis  is  either  a  vascular  lesion  (hemor- 
rhage or  softening),  a  tumor,  or  a  sclerotic  patch.  Which 
of  these  it  is  must  be  decided  by  the  help  of  other  indica- 
tions (see  Chap.  IV.).     A  basal  lesion  is  probably  chronic 


502        DISEASES   OF  THE   NERVOUS   SYSTEM. 

meningitis,  tumor,  or  caries  of  bone.  Paralysis  of  the 
superior  maxillary  division  may  depend  either  on  tumor  or 
cellulitis  of  the  orbit,  or  on  carotid  aneurism,  or  on  a  new 
growth  in  the  pituitary  region.  Paralysis  of  the  second 
and  third  divisions  depends  often  on  tumor  of  the  parotid 
region  or  disease  of  the  antrum.  Sometimes  the  fifth  is 
paralyzed  from  primary  neuritis  and  occasionally  from 
trauma  (as  in  punctured  wounds  through  the  mouth). 

Paralysis  of  the  Facial  Nerve. — Clinically  it  is  impor- 
tant to  distinguish  two  forms  of  facial  paralysis,  viz,  : 

I.  Facial  paralysis  involving  all  the  muscles  supplied  by 
the  facial  nerve  (see  p.  52)  including  the  orbicularis  palpe- 
brarum and  the  frontal  portion  of  the  occipito-f rontalis.  In 
these  cases  of  complete  facial  paralysis  the  voluntary  and 
involuntary  movements  of  the  face  suffer  equally,  and  in 
the  course  of  time  there  are  the  changes  of  electrical  irri- 
tability in  nerve  and  muscle  that  characterize  degenerative 
processes  in  nerves.  In  some  slight  cases  the  electrical 
changes  are  slight  or  absent.  The  senses  of  taste  and  of 
hearing  may  or  may  not  be  affected  in  this  form  of 
paralysis. 

All  cases  of  facial  paralysis  belonging  to  this  group  are 
due  to  disease  of  the  lower  segment  of  the  facial  path, 
/.  <?.,  to  disease  (i)  of  the  facial  nerve  itself  (peripheral 
paralysis),  or  (2)  of  the  nerve  in  its  course  through  the 
pons  to  its  nucleus,  or  (3)  of  its  nucleus  (nuclear 
paralysis). 

II.  Facial  paralysis  in  which  the  muscles  of  the  upper 
part  of  the  face  (orbicularis  palpebrarum,  and  frontalis) 
are  little  or  not  at  all  affected,  and  in  which  the  paralysis 
is  practically  confined  to  the  muscles  about  the  angle  of 
the  jaw. 

In  this  form  of  paralysis  the  voluntary  movements  of 
the  face  are  lost   but  the  emotional  and  reflex  ?noveme?its 


THE  DIAGNOSIS   OF   CLINICAL   TYPES.  503 

of  the  face  are  preserved  or  little  affected.  Moreover,  in 
these  cases  the  electrical  reactions  are  normal  or  only 
slightly  changed  ;  there  is  no  RD.  This  type  of  facial 
paralysis  always  depends  on  disease  of  the  upper  segment 
of  the  facial  path  above  the  facial  nucleus  (supra-nuclear 
paralysis)  either  in  the  pons,  eras,  internal  capsule, 
centrum  ovale,  or  the  cortex  (see  Chaps,  I.  and  III.).  It 
is  generally  associated  with  other  evidences  of  brain  dis- 
ease and  often  forms  part  of  typical  hemiplegia  (p.  74). 
A  rough  diagnosis  of  the  position  of  the  lesion  that 
causes  facial  paralysis  may  be  made  from  the  facts  that 
have  just  been  presented — that  is,  we  may  infer  from  these 
facts  whether  the  disease  is  in  the  upper  or  lower  segment 
of  the  facial  path.  A  more  accurate  localization  must 
depend  on  other  indications.  The  facts  which  relate  to 
the  exact  localization  of  facial  paralysis  from  disease  in 
the  upper  segment  of  the  facial  path  (supra-nuclear  par- 
alysis) have  been  sufficiently  considered  elsewhere  (see 
Localization). 

If  (owing  to  the  correspondence  of  the  symptoms  to 
the  first  type  described)  it  has  been  determined  that  the 
lesion  is  not  supra-nuclear,  an  effort  must  be  made  to 
locate  it  more  exactly  by  the  associations  of  the  paralysis. 
Thus,  if  the  facial  is  the  only  cranial  nerve  paralyzed  and 
the  sense  of  taste  is  normal  on  the  side  of  the  paralysis, 
the  lesion  is  outside  the  stylo-mastoid  foramen  or  just 
within  the  Fallopian  canal  (see  Fig.  54). 

If  the  sense  of  taste  is  involved  on  the  anterior  two 
thirds  of  the  tongue  on  the  side  of  the  lesion,  the  seat  of 
disease  is  in  the  Fallopian  canal  at  some  point  between 
the  junction  with  the  chorda  tympani  and  the  geniculate 
ganglion  (where  the  great  superficial  petrosal  nerve  con- 
taining the  taste-fibres  joins  the  trunk  of  the  nerve  (see 
Fig.  54).    Disease  of  the  nerve  at  the  geniculate  ganglion 


504 


DISEASES   OF  THE   NERVOUS   SYSTEM. 


has  been  thought  to  cause  paralysis  of  the  palate,  but  it  is 
extremely  doubtful  if  this  is  so.  Inequality  of  the  palate 
is  almost  always  congenital  and  has  no  localizing  signifi- 
cance in  cases  of  facial  paralysis.  If  there  is  complete 
deafness  in  the  ear  on  the  side  of  the  lesion,  and  if  this 
deafness  dates  from  the  time  of  the  facial  paralysis,  the 
disease  is  in  the  trunk  at  the  base  of  the  brain,  or  (in 
rare  cases)  in  the  internal  auditory  meatus.     If  paralysis 


5ryi,o-MAsTouD 

EORAIVIEN 


FIG.   54 


Diagram  illustrating  some  of  the  more  important  relations  of  the  facial  nerve 
between  its  superficial  origin  at  the  base  of  the  brain  and  its  division  into 
branches  after  leaving  the  stylo-mastoid  foramen. 

of  the  sixth  nerve  is  associated  with  paralysis  of  the 
facial,  the  lesion  is  no  doubt  in  the  pons,  and  in  all 
probability  in  its  posterior  part,  where  the  fibres  of  the 
seventh  pass  round  the  sixth  nucleus  (see  Fig.  30). 
Crossed  hemiplegia  also  points  to  a  pontine  lesion  (see 
Localization).  Disease  of  the  facial  nucleus  is  probably 
indicated  where  all  muscles  supplied  by  the   nerve  are 


THE   DIAGNOSIS    OF   CLINICAL   TYPES.  505 

paralyzed  except  the  orbicularis  oris  (which  is  probably 
innervated  by  the  twelfth  nerve). 

Facial  paralysis  may  result  from  a  great  variety  of 
morbid  processes.  Some  of  these  may  be  briefly  enu- 
merated. Disease  in  the  pons  (nucleus,  nerve,  or  both) 
may  be  hemorrhage,  acute  softening,  degeneration  (as  in 
bulbar  paralysis),  tumor,  or  inflammation,  as  in  the  rare 
cases  of  facial  paralysis  that  complicate  poliomyelitis. 
Which  of  these  processes  is  operative  in  producing  the 
racial  paralysis  must  of  course  be  determined  by  the 
use  of  other  indications  of  the  nature  of  the  lesion 
(Chap.  IV.).  When  the  paralysis  is  due  to  a  lesion  of 
the  nerve  at  the  base  of  the  brain  the  process  is  usually 
chronic  meningitis  or  tumor.  When  the  paralysis  is  due 
to  disease  in  the  Fallopian  canal  it  may  be  dependent  on 
a  neuritis  from  cold  ("  rheumatic  neuritis  " — very  com- 
mon cause),  or  it  may  depend  on  damage  secondary  to 
ear-disease  (common  cause  in  children),  or  to  pressure  on 
the  nerve  from  fracture  of  the  petrous  portion  of  the 
temporal  bone  in  a  lesion  at  the  base.  Paralysis  from  a 
lesion  outside  the  skull  is  seen  in  some  cases  of  tumor 
of  the  parotid  region,  in  cases  of  wounds  (surgical  or 
accidental)  about  the  ramus  of  the  jaw,  and  in  some 
cases  of  pressure  from  the  forceps  during  delivery. 

Most  of  the  causes  of  facial  paralysis  that  have  been 
mentioned  give  rise  to  one-sided  paralysis,  but  in  rare  in- 
stances double  facial  paralysis  is  seen.  This  occurs  in 
some  cases  of  pontine  disease,  in  certain  cases  of  exten- 
sive disease  (chronic  meningitis)  of  the  base,  in  rare 
cases  of  rheumatic  neuritis,  sometimes  from  double  otitis 
media,  and  occasionally  in  diphtheritic  and  alcoholic 
neuritis,  in  facial  erysipelas,  and  in  bulbar  paralysis. 
There  is  one  point  in  the  diagnosis  of  facial  paralysis 
the  neglect  of  which  (though  it  is  very  elementary)  some- 


5o6         DISEASES   OF  THE   NERVOUS   SYSTEM. 

times  leads  to  error.  During  the  early  stage  of  facial 
paralysis  the  drooping  of  the  mouth  on  one  side  makes 
it  only  too  evident  that  this  is  the  side  paralyzed.  But 
after  the  lapse  of  five  or  six  months,  if  there  is  some 
recovery  of  power,  contracture  develops  in  the  paralyzed 
muscles  (especially  marked  in  the  zygomatici),  and  the 
angle  of  the  mouth  is  drawn  up  on  the  affected  side. 
Hence  an  error  may  be  made  as  to  the  side  affected,  un- 
less the  patient  is  made  to  move  both  sides  of  the  mouth, 
when  it  is  immediately  evident  that  the  palsy  is  on  the 
side  of  the  contracture. 

The  average  duration  of  moderately  severe  cases  of 
'facial  paralysis  is  two  or  three  months.  The  electrical 
reactions  (see  page  190)  afford  the  best  means  of  gauging 
the  severity  of  the  process. 

Facial  Spasm  (tic  convulsive,  mimic  spasm). — This 
name  is  given  to  cases  of  spasm  in  the  muscles  supplied 
by  the  facial  nerve.  The  spasm  is  usually  unilateral  and 
affects  chiefly  the  zygomatici  and  the  orbicularis  palpe- 
brarum. It  is  generally  clonic  in  character,  but  may  be 
tonic,  or  tonic  and  clonic.  Usually  the  disease  is  pri- 
mary. Sometimes,  however,  it  occurs  as  a  result  of  facial 
paralysis. 

Primary  facial  spasm  must  be  distinguished  from  that 
which  is  secondary  to  facial  paralysis,  and  the  distinction 
is  based  chiefly  on  the  absence  of  paralysis  and  on  the 
absence  of  secondary  contracture.  Primary  facial  spasm 
is  easily  distinguished  from  cases  of  chorea  in  which  the 
face  is  chiefly  affected,  by  the  fact  that  in  these  cases  of 
chorea  the  spasm  is  never  confined  to  the  face.  "  Blepha- 
rospasm," or  spasm  limited  to  the  eyelids,  differs  from 
primary  facial  spasm  (though  it  is  indeed  a  variety  of 
such  spasm)  in  its  limitation  to  the  eyelids,  its  bilateral 


THE   DIAGNOSIS   OF  CLINICAL    TYPES.  507 

distribution,  and  its  dependence  upon  a  reduction  in  the 
general  health. 

Having  concluded,  in  a  given  case,  that  the  facial 
spasm  is  primary,  it  is  important  to  determine  the  position 
and  character  of  the  disease.  Facial  spasm  may  occur 
from  disease  of  the  cortical  face  centre,  from  disease 
of  the  facial  nucleus  in  the  pons,  or  from  disease  of  the 
trunk  of  the  nerve.  Sometimes  the  disease  is  organic  in 
nature  ;  more  often  it  is  functional  or  nutritional.  If  paral- 
ysis of  the  facial  muscles  follows  the  spasm,  the  disease 
is  probably  organic,  and  in  such  a  case  other  evidences 
of  an  organic  lesion  are  usually  present.  If  the  spasm 
includes  both  the  corrugators  and  other  facial  muscles 
on  one  side  only,  the  disease  is  probably  cortical.  Cortical 
disease  may,  however,  cause  partial  and  strictly  uni- 
lateral facial  paralysis.  If  the  spasm  appears  due  to  cold 
or  to  neuralgia,  there  is  probably  functional  derangement 
of  the  nucleus.  If  there  is  no  apparent  cause  for  the 
spasm,  or  if  it  appears  related  to  mental  influences  (emo- 
tion, etc.),  the  disease  (nutritional)  is  probably  in  the 
cortical  cells  or  perhaps  in  the  cells  of  the  facial  nucleus. 

Paralysis  of  the  Glosso- Pharyngeal  Nerve. — The  ninth 
nerve  seldom  suffers  alone  and  the  symptoms  of,  its  iso- 
lated paralysis  are  not  definitely  known.  Probably  it 
causes  loss  of  sensibility  and  partial  loss  of  power  in  the 
upper  part  of  the  pharynx.  The  nerve  is  not  rarely  dis- 
eased in  company  with  other  cranial  nerves,  and  is  espe- 
cially apt  to  suffer  in  disease  of  the  nerve-roots  of  the 
medulla  (tumor,  meningitis). 

Paralysis  of  the  Pneumogastric  Nerve. — Owing  to  the 
varied  distribution  of  the  tenth  nerve  disease  involving 
it  may  give  rise  to  many  different  symptoms,  according  to 
the  position  and  nature  of  the  morbid  process.    Generally 


508        DISEASES   OF  THE  NERVOUS   SYSTEM. 

speaking,  the  chief  symptoms  of  paralysis  of  the  nerve 
are  (i)  paralysis  of  the  larynx,  (2)  increased  frequency 
of  the  pulse,  and  (3)  retardation  of  respiration.  With 
these  symptoms  of  paralysis  may  be  associated  the  symp- 
toms of  irritation  of  the  tenth,  of  which  the  chief  are 
(i)  laryngeal  spasm,  and  (2)  vomiting.  Some  of  these 
symptoms  have  been  sufficiently  described  elsewhere  (see 
Laryngeal  Paralysis,  Laryngeal  Spasm,  Cheyne-Stokes' 
Respiration.)  It  is  necessary  to  mention  here  only  two 
other  results  of  pneumogastric  derangement,  paralysis  of 
the  pharynx  and  spasm  of  the  pharynx.  Paralysis  of  the 
pharynx  is  shown  by  the  inability  of  the  patient  to  swal- 
low food,  which,  when  placed  in  the  pharynx  remains 
there.  Pharyngeal  paralysis  may  result  from  disease  of 
the  nuclei  of  the  tenth,  or  from  disease  at  the  base  (menin- 
gitis, tumor),  involving  the  roots  at  the  side  of  the  medulla, 
and  sometimes  from  diphtheric  neuritis.  Unless  the  pha- 
ryngeal nerves  are  involved  on  both  sides  the  difficulty  in 
swallowing  is  slight. 

Spasm  of  the  pharynx  never  results  from  organic  disease. 
In  some  cases  of  hysteria  it  is  associated  with  a  sensation 
as  of  a  large  mass  in  the  pharynx,  known  as  the  "  globus 
hystericus."  Its  nature  is  readily  recognized  by  the 
existence  of  other  hysterical  symptoms.  The  spasm  is 
of  short  duration  in  these  cases.  Pharyngeal  spasm  is 
also  seen  in  some  cases  of  hydrophobia. 

The  diagnosis  of  the  exact  position  of  the  lesion  which 
causes  vagus  paralysis  depends  largely,  as  in  many  other 
cranial  nerve  paralyses,  on  the  associated  conditions. 
The  roots  of  the  nerve  at  the  side  of  the  medulla  and 
the  branches  of  the  nerve  are  much  more  often  the  seat 
of  disease  than  the  trunk  of  the  nerve.  If  the  lesion 
involves  the  roots  at  the  side  of  the  medulla,  there  are 
the  signs   of  implication  of  other  nerves,  especially  the 


THE   DIAGNOSIS    OF   CLINICAL   TYPES.  509 

hypoglossal.  The  recurrent  laryngeal  nerves  are  the 
branches  of  the  vagus  most  often  involved,  and  the  symp- 
toms attending  their  disease  have  been  already  described 
(see  p.  135).  The  causes  of  damage  to  the  vagus  are  nu- 
merous. Disease  of  the  nucleus,  which  is  usually  bilateral, 
may  be  either  softening,  hemorrhage,  or  degeneration,  and 
in  most  cases  is  associated  with  the  signs  of  involvement 
of  adjacent  nuclei  in  the  medulla.  When  the  nerve  is 
injured  at  the  side  of  the  medulla  the  lesion  is  com- 
monly meningitis  or  tumor,  sometimes  vertebral  aneurism. 
The  trunk  of  the  nerve  is  damaged  occasionally  by 
wounds  of  the  neck,  sometimes  inflicted  during  surgical 
operations  ;  sometimes  the  trunk  is  compressed  by  new 
growths  of  the  neck,  enlarged  nodes,  etc.  The  recurrent 
laryngeal  is  often  compressed  by  aneurism  (especially  on 
the  right  side)  within  the  thorax,  and  sometimes  by  cheesy 
nodes  or  new  growths  in  the  chest.  The  diagnosis  in  such 
cases  is  greatly  aided  by  the  presence  of  physical  signs 
of  thoracic  disease,  but  sometimes  such  signs  are  absent 
and  the  diagnosis  is  difficult.  Neuritis  of  the  vagus  is 
the  lesion  in  some  cases  of  diphtheritic  paralysis  (which 
is  very  apt  to  involve  the  vagus)  and  in  the  cases  of  loco- 
motor ataxia  in  which  laryngeal  "  crises  "  occur.  It  is 
said  that  in  rare  instances  exposure  to  cold  may  cause 
symptoms  of  vagus  derangement  from  neuritis  of  the 
trunk. 

Paralysis  of  the  Spinal  Accessory  Nerve. — Paralysis  of 
the  "  accessory  "  portion  of  the  eleventh  nerve  (see  Anat- 
omy) gives  rise  to  paralysis  of  the  larynx  (see  p.  135),  and 
need  not  be  considered  here.  Paralysis  of  the  "spinal" 
portion  of  the  nerve,  which  supplies  the  sterno-mastoid 
and  trapezius  muscles,  causes  characteristic  symptoms 
dependent  on  the  loss  of  function  of  these  muscles. 

Each  sterno-mastoid  muscle  by  its  contraction  rotates 


5IO         DISEASES   OF   THE   NERVOUS   SYSTEM. 

the  face  towards  the  opposite  side,  while  it  draws  down 
the  head  to  the  side  on  which  it  contracts.  If  one 
sterno-mastoid  muscle  is  paralyzed  it  produces  little  or 
no  effect  on  the  position  of  the  head  or  in  its  movements, 
as  the  loss  is  compensated  by  other  muscles.  The  de- 
fective rotation  to  the  opposite  side  may,  however,  be 
easily  determined.  The  unparalyzed  muscle  may  incline 
the  head  to  the  side  opposite  the  paralyzed  muscle,  by 
its  contracture.  The  fact  that  mere  paralysis  of  the 
sterno-mastoid  causes  no  deformity  when  the  head  is  at 
rest  is  of  some  practical  importance.  When  both  sterno- 
mastoids  act  they  support  the  head  in  the  anatomical 
position,  and  when  the  head  is  put  back  they  together 
draw  it  forward.  Paralysis,  therefore,  of  both  sterno- 
mastoids  makes  it  very  difficult  for  the  patient  to  bring 
forward  the  head  when  it  falls  back.  The  sterno-mastoid 
atrophies  when  it  is  paralyzed. 

The  trapezius  consists  of  three  portions,  an  upper,  a 
middle,  and  a  lower  portion.'  Disease  of  the  eleventh 
causes  paralysis  of  the  upper  part  and  partial  paralysis 
of  the  middle  part.  The  upper  part  is  used  mainly  dur- 
ing respiration,  and  its  paralysis  is  shown  chiefly  by  a 
sinking  in  of  the  muscle  which  causes  a  change  in  the 
contour  of  the  neck,  especially  marked  during  deep 
respiration.  Paralysis  of  the  middle  portion  of  the 
trapezius  (which  elevates  the  scapula  and  the  shoulder, 
and  rotates  the  scapula  with  the  lower  angle  out),  causes 
a  dropping  of  the  scapul?  and  shoulder  and  a  rotation  in 
of  the  lower  angle  of  the  scapula,  with  defective  elevation 
of  the  arm.  This  middle  part  of  the  trapezius  is,  how- 
ever, only  partially  paralyzed  in  spinal-accessory  disease. 

'It  is  now  generally  believed  that  branches  from  the  lower  cervical 
and  upper  dorsal  nerves  only  pa^s  through  the  trapezius  muscle,  and 
that  this  muscle  is  wholly  supplied  by  the  spinal  accessor/. 


THE  DIAGNOSIS   OF   CLINICAL  TYPES.         51I 

The  parts  affected  waste  and  show  altered  electrical 
reactions,  which  vary  with  the  character  of  the  disease 
causing  the  paralysis.  Bilateral  trapezius  paralysis  causes 
a  falling  forward  and  sinking  of  the  head,  the  chin  resting 
on  the  sternum. 

The  precise  distribution  of  the  paralysis  of  spinal 
accessory  disease  varies  with  the  position  of  the  lesion. 
When  disease  (usually  degenerative)  involves  gray  matter 
from  which  the  spinal  accessory  arises,  the  paralysis  is 
never  confined  to  the  sterno-mastoid  and  trapezius,  and 
the  affection  is  bilateral  (see  Bulbar  Paralysis).  The  entire 
trapezius  is  usually  involved  in  degenerative  disease  of 
the  gray  substance.  When  the  nerve-trunk  is  the  seat  of 
the  lesion,  the  paralysis  involves  the  sterno-mastoid  and 
the  upper  part  of  the  trapezius.  If  the  spinal  accessory 
nerve  is  damaged  in  its  course  within  the  skull,  both 
portions  of  the  nerve  (spinal  and  accessory)  may  be 
involved.  There  is  then  paralysi.s  of  the  larynx  on  the 
side  of  the  lesion,  in  addition  to  the  muscular  paralyses 
that  characterize  spinal  accessory  disease.  With  these 
symptoms  there  may  be  associated  paralysis  of  one  half 
of  the  tongue,  owing  to  the  proximity  of  the  eleventh  and 
twelfth  nerves.  Paralysis  of  the  palate  (levator  palati) 
on  the  side  of  the  lesion  is  sometimes  seen  in  these  cases, 
and  may  depend  on  disease  of  the  eleventh  or  perhaps 
on  disease  of  the  twelfth  nerve.  When  the  eleventh  nerve 
is  damaged,  as  is  sometimes  the  case,  after  it  has  passed 
through  the  sterno-mastoid,  the  paralysis  is  confined  to 
the  trapezius. 

Spasm  of  the  Muscles  Supplied  by  the  Spinal  Accessory 
iV(?rz^^  ("  Wry-Neck,"  "  Torticollis  ").— The  term  "  wry- 
neck "  is  applied  to  several  different  affections  in  which 
muscular  contraction  produces  an  abnormal  position  of 
the  head.     In  some  cases  the  unnatural  position  of  the 


512         DISEASES  OF  THE  NERVOUS   SYSTEM. 

head  depends  on  persistent  shortening  of  a  muscle  (usu- 
ally the  sterno-mastoid).  Such  cases  are  usually  con- 
genital, and  this  form  of  wry-neck  is  known  as  congenital 
or  fixed  wry-neck.  In  other  cases,  which  are  of  much 
greater  importance  from  a  diagnostic  point  of  view  than 
the  congenital  cases,  the  unnatural  position  of  the  head 
depends,  not  on  muscular  contraction,  but  on  some  quite 
different  condition — usually  on  caries  of  the  upper  cer- 
vical spine.  Such  cases  are  sometimes  spoken  of  as  cases 
of  "  false  wry-neck."  In  a  third  class  of  cases  the  devia- 
tion of  the  head  is  due  to  muscular  rheumatism  (acute 
myositis),  and  the  tender  muscles  are  the  most  important 
cause  of  the  unnatural  fixation  of  the  head.  In  other 
cases  still  wry-neck  is  produced  by  hysterical  spasm. 
None  of  these  cases  will  be  considered  here  except  in  so 
far  as  they  are  liable  to  be  confounded  with  true  wry-neck. 

Spasmodic  or  True  Wry-Neck  depends  on  active  spasm, 
usually  of  the  muscles  supplied  by  the  spinal  accessory 
nerve.  The  cause  of  this  spasm  appears  to  be  a  peculiar 
instability  in  the  nerve-cells  (cortical  or  spinal)  that  con- 
trol the  muscles  involved.  In  no  case  has  an  organic 
lesion  been  detected  as  the  cause  of  the  condition. 

The  distribution  and  character  of  the  spasm  vary  in 
different  cases.  Several  muscles  are  usually  affected, 
most  often  the  sterno-mastoid  and  trapezius  (upper  part) 
of  the  same  side.  Not  rarely  the  spasm  involves  also  the 
splenius,  and  occasionally  the  scaleni  and  platysma  myo- 
ides  are  included.  Sometimes  the  spasm,  which  has  a  ten- 
dency to  extend,  includes  other  muscles  than  those  of  the 
neck,  as  the  muscles  of  the  face,  jaw,  or  arm.  Occasionally 
the  spasm  is  limited  to  one  muscle  of  the  neck,  which  is 
almost  invariably  the  sterno-mastoid,  and  in  rare  cases 
all  the  neck  muscles  participate  in  the  spasm.  Generally 
the  spasm  involves  chiefly  or  exclusively  the  muscles  of 


THE  DIAGNOSIS   OF   CLINICAL  TYPES.  513 

one  side  ;  occasionally  the  muscles  of  both  sides  are 
about  equally  affected. 

Owing  to  such  wide  differences  as  these  in  the  distri- 
bution of  the  spasm,  and  to  similar  differences  in  its 
degree,  the  resulting  change  in  the  position  of  the  head 
varies  much  in  different  cases.  The  chief  positions  ob- 
served are  as  follows  :  {a)  rotation  of  face  to  side  oppo- 
site spasm  and  slight  inclination  of  head  to  side  of 
spasm, — dependent  on  spasm  of  one  sterno-mastoid  ;  {h) 
rotation  of  face  to  side  opposite  spasm  and  great  inclina- 
tion of  head  to  side  of  spasm — dependent  on  spasm  of 
sterno-mastoid  and  trapezius  of  one  side  ;  {c)  extreme 
rotation  of  head  to  one  side,  dependent  on  spasm  of 
sterno-mastoid  of  one  side  and  of  the  splenius  of  the 
other — /.  ^.,  the  side  to  which  the  face  turns  ;  (^)  retro- 
flexion of  head  ("  retrocollic  "  spasm),  due  usually  to 
bilateral  spasm  of  trapezii,  splenii,  and  sterno-mastoid. 
Sometimes  the  spasm  of  torticollis  is  tonic,  at  others 
clonic,  and  sometimes  clonic  and  tonic  spasms  occur 
together.  The  spasm  varies  in  degree  and  character  from 
time  to  time,  and  at  times  there  may  be  short  or  long  in- 
termissions, or  the  spasm  may  be  continuous.  The  onset 
of  the  spasm  is  usually  gradual,  rarely  acute,  and  is  often 
attended  or  preceded  by  pain.  The  muscles  involved 
never  waste,  but  may  hypertrophy  in  time.  Spasmodic 
torticollis  is  usually  a  disease  of  long  duration  and  in 
severe  cases  persists  during  life  with  little  change. 

The  diagnosis  of  spasmodic  wry-neck  is  rarely  difficult. 
Sometimes  it  is  confounded  with  the  false  wry-neck 
already  mentioned,  when,  as  not  rarely  happens,  the  latter 
is  among  the  earliest  evidences  of  caries  of  the  cervical 
spine.  There  are  several  points  of  distinction  between 
wry-neck  of  functional  origin  and  that  which  depends  on 
vertebral  disease,  and  error  may  always  be  avoided  by 


514         DISEASES   OF  THE   NERVOUS   SYSTEM. 

bearing  them  in  mind.  In  spasmodic  wry-neck  the  face  is 
turned  to  the  side  opposite  the  contracting  sterno-mastoid 
muscle.  In  false  wry-neck  the  sterno-mastoid  is  rigid  on 
the  side  to  which  the  face  is  turned.  The  former  condi- 
tion is  painless,  except  at  the  onset ;  in  the  latter  there  is 
often  pain,  neuralgic  in  character,  in  the  distribution  of 
the  sensory  branches  of  the  first  and  second  cervical 
nerves  over  the  occiput.  Moreover,  in  the  latter  condi- 
tion this  pain  is  greatly  aggravated  or  induced  by  sudden 
pressure  on  the  top  of  the  head. 

Hysterical  wry-neck  differs  from  the  true  form  in  that 
the  spasm  rarely  remains  limited  to  the  muscles  of  the 
neck,  in  its  dependence  on  emotion,  in  its  rapid  onset, 
and  in  its  occurrence  in  women  under  thirty  years  of  age, 
before  which  time  true  wry-neck  is  very  uncommon  in 
females. 

Paralysis  of  the  Hypoglossal  Nerve. — The  chief  effect 
of  disease  of  one  hypoglossal  nerve  is  loss  of  power  in 
the  tongue.  When  the  tongue  is  at  rest  in  the  mouth,  its 
base  is  a  little  higher  on  the  paralyzed  than  on  the  un- 
paralyzed  side.  When  the  tongue  is  moved  within  the 
mouth,  there  is  imperfect  power  of  motion  to  the  paralyzed 
side  ;  but  when  the  tongue  \s  protruded,  the  tongue  deviates 
to  the  paralyzed  side,  because  it  is  pushed  to  that  side  by 
the  fibres  of  the  genio-hyo-glossus  on  the  normal  side 
In  disease  of  both  hypoglossal  nerves  the  tongue  cannot 
be  moved  in  the  mouth  and  cannot  be  protruded.  In 
such  cases  there  is  very  defective  articulation. 

Paralysis  of  the  tongue  may  result  from  disease  any- 
where in  the  motor  path  to  the  tongue,  disease  between 
the  cortex  and  the  hypoglossal  nucleus,  disease  of  the 
nucleus,  or  disease  of  the  nerve,  in  or  out  of  the  medulla. 
The  associations  of  the  paralysis  give  the  data  for  the 
localization  of  the  lesion  which  causes  loss   of  power  in 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.  515 

the  tongue.  When  the  disease  is  in  the  upper  segment  of 
the  motor  tract  to  the  tongue, — />.,  is  supra-nuclear,  the 
tongue  paralysis  is  associated  with  hemiplegic  weakness 
on  the  side  of  the  paralysis.  Whether  this  disease  is 
situated  in  the  hemisphere  (including  disease  of  lowest 
part  of  the  third  frontal  convolution),  in  the  crus,  or  in 
the  pons,  must  be  determined  by  other  indications  (see 
Localization,  also  Hemiplegia).  When  disease  involves 
the  nucleus,  the  paralysis  is  bilateral,  owing  to  the  close- 
ness of  the  nuclei  to  one  another  (see  p.  59).  There  is 
also  atrophy  of  the  tongue  in  such  cases,  and  generally 
paralysis  of  the  lips.  Nuclear  disease  is  almost  always 
degenerative  (bulbar  paralysis,  rarely  locomotor  ataxia) 
in  character,  but  may  result  from  vascular  lesions 
(hemorrhage,  softening).  If  the  hypoglossal  fibres  are 
involved  within  the  medulla,  there  is  usually,  but  not 
necessarily,  paralysis  of  the  limbs  on  the  opposite  side 
(crossed  paralysis),  owing  to  the  contiguity  of  the  nerve 
and  the  motor  path.  Both  hypoglossals  may  be  involved 
by  a  bilateral  lesion.  Vascular  lesions  or  tumors  may 
cause  paralysis  from  disease  of  the  fibres  within  the 
medulla.  Disease  of  the  hypoglossal  at  the  side  of  the 
medulla  is  one-sided,  and  is  accompanied  by  damage  to 
the  roots  of  the  spinal  accessory,  which  causes  paralysis 
of  the  larynx  and  palate  on  the  same  side.  Chronic 
syphilitic  meningitis  and  new  growths  are  the  chief  causes 
of  such  paralysis.  The  tongue  wastes  to  some  extent  in 
disease  of  any  part  of  the  lower  segment  of  the  path  to 
the  tongue-nucleus,  nerve,  or  path  in  the  medulla  between 
nucleus  and  nerve. 

Spasm  of  the  tongue,  causing  its  deviation  to  one  side 
on  protrusion  is  occasionally  met  with  as  a  symptom  of 
hysteria.  It  then  is  usually  associated  with  other  more 
distinctive  signs  of  this  disease,  especially  convulsion,  but 
may  occur  apart  from  any  other  spasmodic  symptoms. 


5l6        DISEASES   OF   THE   NERVOUS   SYSTEM. 

Paralysis  of  the  Phrenic  Nerve} — The  consequence 
of  paralysis  of  the  functions  of  the  phrenic  nerve  is  in- 
action of  the  diaphragm.  If  the  paralysis  is  unilateral 
the  diaphragm  does  not  descend  on  that  side  during 
inspiration,  but  the  loss  of  movement  is  not  considerable, 
as  the  other  side  of  the  diaphragm  continues  to  act. 
When  both  phrenics  are  paralyzed  the  inaction  of  the 
diaphragm  produces  a  decided  effect  upon  respiration. 
The  movement  of  the  thorax  is  increased,  but  if  the  hand 
is  placed  on  the  abdomen  below  the  ribs,  the  advance  of 
the  abdominal  wall  and  the  descent  of  the  viscera  which 
occurs  during  normal  inspiration  can  no  longer  be  felt. 

The  phrenic  nerve  may  be  paralyzed  from  disease  or 
injury  of  the  spinal  cord  (most  common  cause),  from 
damage  to  the  roots  of  the  nerve,  and  from  disease  or 
injury  to  the  nerve  trunk,  either  in  the  neck  or  thorax. 
When  the  paralysis  depends  on  cord  disease,  it  is  bilateral, 
and  other  paralyses  are  associated  with  that  of  the  dia- 
phragm. Compression  and  crush  of  the  cord  are  the 
most  frequent  causes  of  such  paralysis.  When  the  nerve 
trunk  is  the  seat  of  the  lesion  only  the  diaphragm  suffers 
and  the  paralysis  is  generally  unilateral.  The  nerve  may 
suffer  in  the  neck  from  deep  wounds,  or  in  the  thorax 
from  tumors  or  aneurisms.  Sometimes  it  is  the  seat  of 
neuritis  from  cold  or  from  diphtheria,  and  the  paralysis 
may  then  be  bilateral. 

In  some  cases  of  hysteria  the  diaphragm  may  be  little 
used  for  a  considerable  period  of  time,  the  upper  part  of 
the  thorax  acting  as  when  the  diaphragm  is  paralyzed. 
Knowledge  of  this  fact  and  the  detection  of  activity  of 
the  diaphragm  will  avoid  an  error,  but  it  may  be  necessary 
to  observe  for  some  time  before  forming  an  opinion. 

'  The  plirenic  nerve  is  derived  from  the  third,  fourth,  and  fifth 
cervical  nerves. 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.  517 

The  movements  of  the  diaphragm  are  arrested  or 
diminished  in  some  cases  of  diaphragmatic  pleurisy,  but 
the  pain  which  accompanies  this  condition  will  serve  to 
prevent  an  error  in  diagnosis. 

Paralysis  of  the  Posterior  Thoracic  Nerve} — Damage 
to  the  posterior  thoracic  nerve  results  in  paralysis  of  the 
serratus  magnus  muscle.  The  chief  effects  of  this  paralysis 
are  :  (i)  rotation  of  the  scapula  on  its  vertical  axis  when 
the  arm  is  put  forward,  with  recession  of  the  edge  of  the 
scapula  from  the  thorax — so-called  "winged  scapula" 
(this  is  characteristic  of  serratus  paralysis)  ;  (2)  the 
lower  angle  of  the  scapula  is  rotated  inward  and  upward 
when  the  arm  is  carried  forward  ;  (3)  the  power  of  elevat- 
ing the  arm  above  the  level  of  the  shoulder  is  greatly 
weakened.  There  is  usually  severe  pain  in  the  neck  and 
shoulder  during  the  development  of  the  paralysis. 

The  evidences  of  isolated  serratus  paralysis  are  so  char- 
acteristic that  an  error  in  diagnosis  is  scarcely  possible. 
The  nerve  is  usually  damaged  in  the  neck,  either  by  direct 
pressure  of  heavy  angular  objects  on  the  shoulder  or  by 
violent  muscular  effort  as  in  lifting  a  heavy  hammer.  Some- 
times it  is  injured  by  a  wound  or  contusion.  In  rare  cases 
the  paralysis  follows  exposure  to  cold.  Isolated  serratus 
paralysis  is  usually  one-sided;  rarely  it  is  bilateral.  It  is 
much  more  common  in  men  than  in  women,  and  is  gener- 
ally on  the  right  side,  as  seen  in  Fig.  57?  Sometimes  the 
posterior  thoracic  nerve  is  paralyzed  from  disease  of  its 
cells  of  origin  in  the  cord,  as  in  progressive  muscular 
atrophy  and  infantile  paralysis,  or  crush  of  the  cord. 
Other  muscles  than  the  serratus  are  then  paralyzed  and 
the  nature  of  the  affection  is  plain. 

^  This  nerve  is  derived  from  the  fifth  and  sixth  cervical  nerves. 


5l8         DISEASES   OF   THE   NERVOUS   SYSTEM. 

Paralysis  of  the  Supra- Scapular  Nerve.^ — Damage  tc 
the  supra-scapular  nerve  causes  paralysis  of  the  supra- 


FIG.  57. 

Position  of  shoulder-blades  in  paralysis  of  the  right  serratus  magnus  during 
abduction  of  the  arms. 

spinatus    and  infra-spinatus  muscles.     The    paralysis  of 

the   former  gives    rise   to    no    obtrusive    symptoms,  but 

'  This  nerve  is  derived  from  the  fourth  and  fifth  cervical  nerves. 


THE  DIAGNOSIS   OF   CLINICAL  TYPES.  519 

paralysis  of  the  infra-spinatus  causes  a  loss  of  outward 
rotation  of  the  humerus.  An  important  effect  of  this 
loss  is  the  inability  to  carry  the  hand  from  left  to  right  as 
in  writing. 

There  is  seldom  isolated  paralysis  of  the  supra-scapu- 
lar nerve,  but  it  is  often  affected  together  with  the  cir- 
cumflex in  consequence  of  dislocation  of  the  head  of  the 
humerus,  and  in  obstetrical  paralysis. 

Paralysis  of  the  Circumflex  Nerve  ^  causes  loss  of  power 
in  the  deltoid  and  teres  minor  muscles.  The  paralysis  of 
the  former  is  by  far  the  more  important.  Its  chief  sign 
is  inability  to  raise  the  arm.  In  some  cases  there  is  loss 
of  sensation  on  the  outside  of  the  upper  part  of  the  arm 
over  the  muscles.  The  deltoid  wastes,  and  this  alters  the 
contour  of  the  shoulder.  After  a  time  trophic  changes 
occur  in  the  shoulder  joint  (the  circumflex  sends  filaments 
to  the  joint),  and  adhesions  may  form.  Paralysis  of  the 
circumflex  nerve  is  easily  recognized.  It  is  impossible  to 
confound  it  with  the  loss  of  motion  that  is  seen  in 
anchylosis  of  the  shoulder  joint,  if  it  is  remembered  that 
in  the  latter  state  passive  motion  of  the  arm  moves  the 
scapula  as  well  as  the  arm.  The  circumflex  nerve  is 
often  injured  by  falls  on  the  shoulder  and  by  dislocations 
of  the  head  of  the  humerus.  Rarely  it  is  the  seat  of 
"  spontaneous  "  neuritis.  It  is  sometimes  paralyzed  with 
other  nerves  belonging  to  the  brachial  plexus  (see  Brachial 
Plexus,  Diseases  of)  in  a  highly  characteristic  manner. 

Paralysis  of  the  Musculo- Cutaneous  Nerve  (External 
Cutaneous,  Perforans  Casserii)  causes  loss  of  power  in 
the  biceps  and  brachialis  anticus  muscles,  the  effects  of 
which  are  unmistakable  (loss  of  flexion  of  elbow — espe- 
cially marked  when  the  forearm  is  supinated  and  the  supi- 

'  This  nerve  is  derived  from  the  fifth,  sixth,  seventh,  and  eighth 
cervical  nerves. 


520         DISEASES   OF  THE   NERVOUS   SYSTEM. 

nator  longus  cannot  act  as  a  flexor).  There  may  or  may 
not  be  anaesthesia  on  the  outer  half  of  the  forearm  in  front 
and  behind,  and  over  the  arm  in  its  lower  part  and  outer 
side.  The  musculo-cutaneous  is  rarely  paralyzed  by 
itself. 

Paralysis  of  the  Musculo- Spiral  Nerve '  in  the  vicinity 
of  the  brachial  plexus  causes  loss  of  power  in  all  the  ex- 
tensors of  the  forearm  and  wrist  and  the  supinators. 
Extension  of  the  elbow  is  impossible,  the  wrist  drops, 


FIG.   58. 

Paralysis  of  the  musculo-spiral  nerve  ;  maximum  extension  of  wrist  and  fingers. 

The  extension  of  the  fingers  progressively  diminishes  from  the  first  to 

the  fourth.     From  a  photograph.     (Gowers.) 

and  the  fingers  are  flexed  at  their  distal  joints.  The 
fingers  can,  however,  be  extended  by  the  interossei  and 
lumbricales  if  the  first  phalanges  are  flexed.  Supination, 
though  not  entirely  lost  (the  biceps  being  active),  is 
greatly  weakened.  After  a  time  the  excessive  flexion 
of  the  carpus  leads  to  undue  prominence  of  the  carpal 
bones  and  the  synovial  sacs  at  the  back  of  the  wrist. 
When  the  damage  to  the  nerve  is  serious  there  is  in  a  few 
weeks  a  perceptible  diminution  in  the  size  of  the  fore- 

'  This  nerve  comes  from  the  fifth,  sixth,  seventh,  and  eighth  cer- 
vical nerves. 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.         521 

arm,  due  to  the  atrophy  of  the  paralyzed  extensors,  and 
the  muscles  present  the  RD  in  various  degrees. 

If  the  damage  to  the  nerve  is  in  the  middle  of  the  arm 
the  biceps  is  generally  involved.  The  supinator  longus 
escapes  only  in  rare  cases  of  musculo-spiral  paralysis. 

The  loss  of  sensation  in  the  parts  supplied  by  the  mus- 
culo-spiral varies  considerably  in  different  cases.  In 
actual  division  of  the  nerve  above  its  cutaneous  branches 
there  is  usually  loss  of  sensation  in  the  outer  part  of  the 
arm  (about  one  quarter  its  circumference)  from  the  level 
of  insertion  of  the  deltoid  to  the  external  condyle  of  the 
humerus,  and  on  the  back  of  the  forearm  on  the  outer 
side  above,  fading  into  normal  sensation  in  the  lower 
third  of  the  forearm.  The  skin  on  the  dorsal  surface  of 
the  hand  is  anaesthetic  over  the  thumb  and  metacarpal 
bones  of  the  thumb,  index,  and  middle  fingers.  In 
many  cases  of  musculo-spiral  paralysis  there  is  no  anaes- 
thesia either  in  the  hand  or  arm. 

Musculo-spiral  paralysis  is  of  frequent  occurrence,  the 
course  of  the  nerve  exposing  it  to  various  kinds  of  injury. 
High  up  the  nerve  may  be  damaged  by  the  pressure  of  a 
crutch.  Indeed,  crutch-paralysis  is  usually  due  to  mus- 
culo-spiral injury.  The  nerve  is  apt  to  be  torn  in  cases 
of  fracture  of  the  humerus,  and  may  be  pressed  upon 
by  callus.  The  most  common  cause  of  the  paralysis, 
however,  is  pressure  on  the  nerve  during  sleep.  The 
patient  lies  on  a  hard  bed  or  on  the  floor  with  the  arm 
under  him  and  receiving  his  weight.  The  nerve  suffers 
as  it  passes  around  the  humerus  about  the  middle  of 
the  arm.  So  often  does  this  occur  in  patients  who  have 
fallen  asleep  after  excess  in  alcohol  that  it  is  known  as 
"Saturday-night  paralysis,"  or  "  Sunday-morning  paraly- 
sis," from  the  times  at  which  the  paralytic  effects  are 
usually  detected. 


522         DISEASES   OF  THE   NERVOUS   SYSTEM. 

It  is  necessary  to  distinguish  musculo-spiral  paralysis 
from  some  forms  of  multiple  neuritis — notably  from  lead 
paralysis  and  alcoholic  neuritis.  In  lead  paralysis  the  mus- 
cles supplied  by  the  musculo-spiral  nerve  are  involved  [vide 
Lead  Paralysis),  but  the  affection  is  almost  invariably  bi- 
lateral (though  the  two  sides  may  suffer  very  unequally), 
and  the  supinator  longus  muscle  is  almost  always  ex- 
empted from  the  palsy.  In  musculo-spiral  paralysis,  on 
the  contrary,  the  paralysis  involves  only  one  nerve  (in 
rare  cases  a  cause  of  musculo-spiral  paralysis  operates 
bilaterally),  and  the  supinator  longus  is  almost  invariably 
included  in  the  palsy.  Moreover,  the  onset  of  lead  palsy 
is  gradual  and  the  development  of  musculo-spiral 
paralysis  is  rapid  or  sudden.  The  cause  of  musculo-spiral 
paralysis  is  usually  readily  elicited.  The  distinction  from 
alcoholic  neuritis  is  usually  extremely  easy  (see  Alcoholic 
Neuritis).  The  bilateral  character  of  the  paralysis,  its 
extensive  distribution,  and  the  alcoholic  history  will 
prevent  error  even  when  the  paralysis  affects  chiefly  the 
upper  extremities. 

Paralysis  of  the  Median  Nerve } — Severe  damage  to  the 
median  nerve  above  its  muscular  branches  causes  loss  of 
power  in  the  flexors  of  the  fingers  (excepting  the  ulnar 
half  of  the  flexor  profundus),  in  the  pronators,  in  the 
flexor  carpi  radialis,  in  the  two  outer  lumbricales,  and 
in  all  the  muscles  of  the  ball  of  the  thumb  except  the  ab- 
ductor pollicis  and  the  ulnar  half  of  the  flexor  brevis 
pollicis.  In  consequence  of  this  loss  of  power  the  ability 
to  flex  and  pronate  the  forearm  is  greatly  diminished  but 
not  abolished.  Flexion  at  the  wrist  to  the  ulnar  side  is 
still  possible  by  the  action  of  the  flexor  carpi  ulnaris  ;  pro- 
nation is  feebly  performed  by  permitting  the  weight  of 
the  hand  to   rotate    the  forearm  after  it  has  been  supi- 

^  This  nerve  arises  from  all  the  roots  of  the  Ijrachial  plexus. 


THE   DIAGNOSIS   OF   CLINICAL   TYPES. 


523 


nated,  the  supinator  longus  being  capable  only  of  pronating 
the  arm  to  a  position  midway  between  supination  and  pro- 
nation. The  thumb  is  extended  and  abducted  in  a  char- 
acteristic manner,  and  cannot  be  brought  in  contact  with 
the  tips  of  the  fingers.  The  second  phalanges  can  no 
longer  be  flexed  on  the  first,  and  in  the  first  and  second 


FIG.    55. 

Diagram  illustrating  the  area  of 
anaesthesia  in  a  case  of  injury  to  the 
median  nerve.     (Palmar  surface.) 


FIG.    56. 

Diagram  illustrating  the  area  of 
anaesthesia  in  a  case  of  injury  to  the 
median  nerve.     (Dorsal  surface.) 


fingers  there  is  also  loss  of  flexion  of  the  third  phalanges. 
The  first  phalanges  are  flexed  by  the  interossei.  The 
characteristic  distribution  of  anaesthesia  which  is  observed 
in  cases  of  injury  to  the  median  nerve  is  sufliciently  well 
shown  in  the  accompanying  diagrams. 

The  degree  and  extent  of  the  anaesthesia  vary  much  in 


524         DISEASES   OF   THE   NERVOUS   SYSTEM. 

different  cases.  Sometimes  there  is  no  affection  of  sensa- 
tion whatever.  In  a  case  of  severe  damage  to  the  median 
the  appearance  of  the  hand  and  forearm  soon  becomes 
highly  characteristic.  The  forearm  is  much  atrophied 
on  the  radial  side  in  front,  the  wrist  is  inclined  to  the 
ulnar  side  and  perhaps  hyper-extended,  the  ball  of  the 
thumb  is  greatly  wasted,  the  head  of  the  metacarpal 
bone  is  prominent,  and  the  thumb  is  usually  rotated  out, 
so  that  its  palmar  surface  is  on  a  plane  with  that  of  the 
hand,  as  is  the  case  in  apes. 

The  median  nerve  is  often  injured.  It  suffers  most 
frequently  just  above  the  wrist-joint,  where  it  is  more 
superficial  than  in  the  rest  of  its  course,  and  is  readily 
divided.  It  may,  however,  be  damaged  in  almost  any 
part  of  its  course.  In  the  forearm  it  is  not  rarely  injured 
in  fractures  of  the  ulna  and  radius.  In  the  upper  arm  it 
is  most  often  invaded  just  above  the  bend  of  the  forearm. 
It  is  said  to  be  in  some  cases  the  seat  of  primary  neuritis. 
Very  rarely  it  is  injured  by  violent  contraction  of  the  pro- 
nator radii  teres. 

Paralysis  of  the  Ulnar  Nerve. — When  the  ulnar  nerve 
is  divided  or  severely  damaged  above  the  origin  of  all  its 
branches,  there  is  loss  of  power  in  the  ulnar  half  of  the 
flexor  profundus  digitorum,  in  the  flexor  carpi  ulnaris,  in 
all  the  muscles  of  the  little  finger,  in  all  the  interossei, 
in  the  two  ulnar  lumbricales,  in  the  abductor  pollicis 
and  in  the  inner  head  of  the  flexor  brevis  pollicis. 
When  this  paralysis  has  lasted  some  time  (three  or  four 
weeks  or  longer),  the  action  of  the  unparalyzed  opposing 
muscles  brings  the  hand  into  a  very  characteristic  posi- 
tion. The  wrist  is  slightly  bent  backwards  and  to  the 
radial  side  of  the  forearm,  by  the  action  of  the  extensor 
carpi  radialis,  extensor  carpi  ulnaris  and  flexor  carpi 
radialis.     The  hand  is  considerably  thinner  than  normal 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.  525 

owing  to  the  wasting  of  the  interossei  and  the  muscles 
of  the  little  finger,  which  leave  the  metacarpal  bone  of 
that  finger  very  prominent.  There  are  depressions  be- 
tween the  metacarpal  bones,  but  there  is  a  particularly- 
marked  depression  on  the  radial  side  of  the  metacarpal 
bone  of  the  index  finger  on  the  back  of  the  hand,  owing 
to  the  wasting  of  the  first  dorsal  interosseus. 

The  paralysis  of  the  interossei  leads  to  a  deformity 
which  is  almost  distinctive  of  ulnar  paralysis.  The  fin- 
gers cannot  be  flexed  at  the  first,  or  extended  at  the 
second  and  third  phalanges,  and,  in  consequence  of  this, 
the  opponents  of  the  interossei  (extensor  communis 
digitorum)  by  their  contracture  over-extend  the  first  pha- 
langes and  flex  the  second  and  third. 

This  deformity  of  the  hand  is  known  as  the  "  bird-claw 
hand,"  or  the  "claw-like  hand."  ^  The  deformity  is 
especially  marked  in  the  third  and  fourth  fingers  ;  the 
first  and  second  are  less  affected  because  their  lumbri- 
cales  escape  paralysis.  This  deformity  occurs  not  only 
when  the  ulnar  nerve  is  damaged  high  up  above  its  mus- 
cular branches,  but  also  in  injuries  at  the  wrist,  though  it  is 
perhaps  less  extreme  in  the  latter  class  of  cases. 

The  state  of  sensation  in  ulnar  paralysis  varies  consid- 
erably ;  in  some  cases  there  is  no  anaesthesia,  in  others, 
of  severe  damage  to  the  nerve,  the  loss  may  be  that  in- 
dicated in  figures  57  and  58 — a  typical  distribution  of 
anaesthesia. 

The  ulnar  nerve  is  probably  more  often  damaged  than 
any  other  spinal  nerve.  It  is  frequently  injured  in 
wounds  of  the  forearm,  especially  in  wounds  at  the  wrist, 
where  the  nerve  is   superficial.     When   the   nerve   is  in- 

^  It  is  seen  also  in  progressive  muscular  atrophy,  where  disease 
affects  the  cells  of  origin  of  the  ulnar  nerve  before  those  of  the  mus- 
culo-spiral. 


526 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


Jured  at  the  wrist  it  is  generally  above  the  origin  of  the 
dorsal  cutaneous  branch.  Higher  up  in  the  forearm  the 
nerve  may  be  hurt  by  fractures  of  the  ulna  and  radius.  At 
the  back  of  the  elbow,  just  external  to  the  olecranon,  the 
nerve  is  very  liable  to  suffer  from  wounds,  and  is  occasion- 
ally injured   by  pressure  or  contusion.     Long-continued 


FIG.   57. 

Diagram  illustrating  area  of  anaes- 
thesia and  position  of  fingers  in  a  case 
of  injury  to  the  ulnar  nerve.  (Dorsal 
surface.)     After  Bowlby. 


Diagram  illustrating  area  of  anaes- 
thesia and  position  of  fingers  in  a  case 
of  injury  of  the  ulnar  nerve.  (Palmar 
surface.) 


flexion  at  the  elbow  sometimes  suffices  to  cause  ulnar  paral- 
ysis. Sometimes  paralysis  arises  in  this  way  during  sleep. 
The  nerve  is  very  rarely  injured  in  the  arm  above  the 
elbow.  Sometimes  the  symptoms  of  an  apparently  spon- 
taneous ulnar  neuritis  are  observed  in  persons  in  reduced 

health. 

32 


THE  DIAGNOSIS   OF   CLINICAL  TYPES.  527 

The  diagnosis  of  ulnar  paralysis  is  simple.  Error  may 
possibly  arise  in  rare  cases  of  disease  of  the  cervical 
enlargement,  in  which  the  ulnar  nerve  distribution  is 
chiefly  affected.  Other  evidences  of  spinal  cord  disease 
are  never  wanting  in  these  cases. 

Paralysis  in  the  Distribution  of  Two  or  More  Nerves  of 
the  Arm^  and  due  to  disease  outside  the  spinal  canal,  is 
not  very  uncommon. 

Thus,  the  median  and  ulnar  nerves  not  rarely  suffer 
together  in  fractures  of  the  ulna  and  radius,  and  in 
wounds  at  the  wrist ;  the  musculo-spiral  and  ulnar, 
sometimes  the  musculo-spiral,  ulnar  and  median,  in 
fractures  of  the  humerus  ;  and  any  or  all  of  the  nerves  of 
the  brachial  plexus  (usually  including  the  circumflex)  may 
be  compressed  or  lacerated  by  dislocation  of  the  humerus 
(especially  sub-coracoid  dislocation}.  Inflammation  may 
ascend  one  nerve  and,  reaching  the  brachial  plexus, 
spread  to  others  ("  ascending  neuritis,"  "  neuritis  mi- 
grans ").  Thus  the  ulnar  may  be  implicated  by  an  as- 
cending median  neuritis  ;  and  conversely,  the  median 
may  be  involved  by  an  ascending  ulnar  neuritis.  The 
original  wounds  are  usually  infected  in  such  cases. 

In  cases  where  nerves  of  the  arm,  and  especially  of  the 
forearm,  have  been  injured,  and  tendons  and  muscles 
have  been  injured  with  the  nerves,  it  may  be  difiicult  to 
distinguish  the  effects  of  the  nerve  injury  and  the  effects 
of  injury  to  the  tendons  and  muscles.  This  is  because 
there  is  often  considerable  cicatricial  change  in  muscles 
and  tendons,  leading  to  deformity,  which  may  simulate 
closely  that  of  nerve  injury,  and  because  certain  of  the 
most  important  signs  of  nerve  injury,  namely,  changes  in 
the  irritability  of  muscles  and  nerves,  may  be  obscured 
by  the  contraction  that  sets  in.  Even  the  most  careful 
attention  to  every  detail  in  the  history  and  examination 


528         DISEASES   OF   THE   NERVOUS   SYSTEM. 

of  such  cases  may  not  enable  the  observer  to  arrive  at  a 
correct  conclusion  as  to  the  extent  and  situation  of  the 
nerve  damage. 

Non- Traumatic  or  Primary  Brachial  Neuritis  is  an 
uncommon  condition  in  which  the  cords  of  the  brachial 
plexus  become  the  seat  of  an  unevenly  distributed  inflam- 
matory process.     The  symptoms  vary  much  in  different 


FIG.  59.  FIG.  60. 

Diagram  illustrating  the  area  of  anaes-  Diagram  illustrating  the  area  of  an- 

thesia  in  a  case  of  injury  to  the  ulnar  sesthesia  in  a  case  of  injury  to  the  ulnar 
and  median  nerves.     (Palmar  surface.)        and  median  nerves.     (Dorsal  surfa«e.) 

cases,  according  to  the  distribution  of  the  neuritis  and  its 
intensity.  The  earliest  symptoms  are  sensory  in  character, 
and  include  pain,  parsesthesia  and  anaesthesia  of  irregu- 
lar distribution.  The  pain  is  usually  referred  to  the 
shoulder ;  sometimes  also  to  the  hand  and  fingers. 
These   sensory  symptoms  may  be  followed  by  gradual 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.  529 

loss  of  power  in  certain  muscles  and  muscular  atrophy. 
The  muscles  suffer  unequally  and  present  various  grades 
of  RD,  but  rarely  the  complete  form.  Vaso-motor  and 
trophic  symptoms  may  occur  but  are  only  rarely  very 
decided.  This  form  of  brachial  neuritis  appears  to  de- 
pend, in  some  cases,  on  exposure  to  cold  or  over-exertion. 
Its  diagnosis  is  simple  if  its  occurrence  is  borne  in  mind. 

ErFs  Paralysis  (obstetrical  palsy). — These  names  are 
given  to  a  peculiar  form  of  paralysis  dependent  on 
damage  principally  to  the  fifth  and  sixth  cervical  nerves 
at  one  point  in  the  neck,  just  in  front  of  the  edge  of  the 
trapezius.  The  paralysis  involves  regularly  the  deltoid, 
biceps,  brachialis  anticus  and  supinator  brevis,  and 
supra-  and  infra-spinati.  There  is  often  anaesthesia  on 
the  outer  side  of  the  arm  in  the  distribution  of  the  cir- 
cumflex and  external  cutaneous  nerve;  there  is  usually 
considerable  muscular  atrophy.  The  characters  of  Erb's 
paralysis  differ  considerably  in  adults  and  young  chil- 
dren. In  adults  the  paralysis  is  often  complete,  sensory 
symptoms  are  marked,  and  the  affection  is  frequently  of 
long  duration.  The  cause  of  the  paralysis  in  adults  is 
usually  a  trauma,  but  sometimes  the  condition  depends 
on  the  presence  of  a  cervical  tumor,  and  occasionally  the 
paralysis  develops  without  known  cause. 

Erb's  paralysis  is  probably  much  more  often  seen  in 
infants  than  in  adults,  but  even  in  them  it  is  an  uncom- 
mon form  of  paralysis.  It  always  depends,  in  infants,  on 
undue  stretching  of  the  nerve  trunks,  during  delivery, thus 
causing  stretching  and  rupture  of  the  nerve  sheaths  and 
trunk.  Hence  it  is  commonly  termed  "obstetrical  paral- 
ysis." ^     The  severity  of  the  damage  to  the  nerves  varies 

'  This  term  is  sometimes  applied  to  the  facial  paralysis  that  arises 
from  the  pressure  of  forceps,  and  to  some  forms  of  infantile  cerebral 
palsy.     A  better  name  is  "  brachial  birth  palsy." 


530         DISEASES   OF  THE   NERVOUS   SYSTEM 

much  in  different  cases.  In  the  slighter  cases  of  injury  tht 
paralysis  may  be  unnoticed  for  some  time  after  the  birth 
of  the  child.  In  a  well  developed  case  the  paralysis  can 
hardly  escape  detection,  and  is  so  peculiar  in  distribution 
as  to  assert  its  nature.  The  arm  hangs  by  the  side  with 
the  forearm  in  extreme  pronation,  or  some  power  of  elbow 
flexion  may  remain.  Atrophy  of  the  paralyzed  muscles  can- 
not be  distinguished  until  several  months  after  the  dam- 
age, and  may  appear  very  slight  even  then,  as  it  is  masked 
by  the  large  amount  of  fat  over  the  muscles.  Sensation  is 
rarely  impaired,  and  when  it  is  the  impairment  may  be 
detected  with  difficulty.  The  paralysis  in  mild  cases 
usually  wears  away  in  the  course  of  a  few  months,  some- 
times in  a  few  weeks,  but  in  all  severe  cases  some  pa- 
ralysis, atrophy,  and  deformity  usually  remain.  The 
peculiar  distribution  of  the  paralysis  and  detection  of 
the  lesion  of  connective  tissue  overgrowth  at  Erb's  point 
by  means  of  palpation,  and  its  occurrence  during  de- 
livery, if  this  can  be  established,  make  the  diagnosis 
clear.  Some  care  must  be  taken  not  to  confound  this 
condition  with  some  forms  of  poliomyelitis  {vide  p.  452), 
or  with  injuries  to  the  shoulder-joint  or  muscles.  The 
characteristic  electrical  reactions  in  the  paralyzed  muscles 
serve  to  distinguish  Erb's  paralysis  from  all  conditions 
outside  the  nervous  system. 

The  nerves  of  the  lower  extremity  are,  on  the  whole, 
less  frequently  the  seat  of  injury  and  disease  than  those 
of  the  upper  extremity. 

Paralysis  of  the  Obturator  Nerve '  gives  rise  to  loss  of 
power  in  the  adductors  of  the  thigh,  and  to  defective 
outward  rotation  of  the  thigh.  The  defective  power  of 
adduction  renders  the  patient  unable  to  cross  the  leg 
of  the  paralyzed  side  over  the  other  leg.  The  obturator 
nerve  is  seldom  paralyzed  except  from  damage  to  the 

^  Derived  from  the  third  and  ft^urth  lumbar  nerves. 


THE   DIAGNOSIS   OF   CLINICAL  TYPES,  53 1 

lumbar  plexus.  Occasionally,  however,  the  nerve  itself 
is  damaged  by  pressure  against  the  pelvis  during 
delivery. 

Paralysis  of  the  Anterior  Crural  Nerve  causes  loss  of 
power  and  atrophy  in  the  extensors  of  the  knee,  and  loss 
of  knee-jerk  from  damage  to  the  reflex  arc.  When  the 
nerve  is  damaged  within  the  pelvis  the  branch  to  the 
iliacus  muscle  is  involved  and  there  is  impaired  ^  power 
of  flexing  the  hip,  as  well  as  loss  of  extension  of  the 
knee.  Paralysis  of  the  anterior  crural  nerve  causes  also 
anaesthesia,  which  involves  the  entire  thigh,  with  the 
exception  of  a  strip  of  variable  width  along  the  back  of 
the  thigh  (supplied  by  the  sacral  nerves)  and  the  inner 
side  of  the  leg  and  foot.  The  anterior  crural  nerve  may 
be  damaged  in  the  thigh  or  groin,  may  suffer  from  pres- 
sure during  parturition,  or  from  dislocation  of  the  hip, 
or  may  be  involved  by  disease  affecting  the  lumbar 
plexus. 

Paralysis  of  the  Superior  Gluteal  Nerve  ^  causes  loss  of 
abduction  and  circumduction  of  the  thigh,  from  paralysis 
of  the  gluteus  minimus  and  medius.  As  an  isolated 
paralysis,  apart  from  affections  of  the  plexuses,  it  is  a 
very  rare  condition. 

Paralysis  of  the  Sciatic  Nerve  causes  symptoms  which 
vary  considerably  with  the  seat  of  the  lesion.  Damage  to 
the  nerve  is  usually  below  the  upper  third  of  the  thigh, 
and,  if  severe,  gives  rise  to  paralysis  of  all  the  muscles 
below  the  knee  and  anaesthesia  of  the  sole  and  outer 
side  of  the  foot  and  the  outer  side  of  the  leg.  The  gait 
in  such  cases  is  much  like  that  observed  in  many  cases 
of  poliomyelitis  in  children.  If  the  lesion  is  above  the 
middle  third  of  the  thigh   the  flexors   of   the  knee   and 

^  Flexion  is  merely  impaired  because  the  psoas  is  supplied  by  other 
lumbar  nerves. 

^  This  nerve  is  derived  from  the  lumbo-sacra]  cord. 


532         DISEASES   OF   THE   NERVOUS   SYSTEM. 

extensors  of  the  hip  are  included  in  the  paralysis.  The 
sciatic  nerve  external  to  the  pelvis  may  be  damaged  in 
wounds  of  the  thigh,  by  disease  of  the  femur,  by  adjacent 
tumors,  and  occasionally  by  dislocation  of  the  hip.  The 
nerve  is  often  the  seat  of  primary  neuritis. 

Paralysis  of  the  External  Popliteal  (Peroneal)  Nerve 
causes  loss  of  power  in  the  tibialis  anticus,  extensor  longus 
digitorum,  extensor  brevis  digitorum  and  peronei,  in 
consequence  of  which  there  is  loss  of  flexion  of  the 
ankle  and  of  extension  in  the  first  phalanges  of  the  toes. 
The  patient  in  such  cases  has  "  drop-foot,"  and  in  the 
.course  of  time  talipes  equinus  develops.  In  cases  of 
severe  damage  to  the  nerve  there  is  anaesthesia  on  the 
outer  half  of  the  front  of  the  leg,  and  on  the  greater  part 
of  the  back  of  the  foot.  The  external  popliteal  nerve  is 
very  superficial  in  its  course,  and  passes  over  the  fibula. 
It  is  consequently  exposed  to  all  kinds  of  injury — from 
wounds,  from  fracture  of  the  fibula,  from  pressure,  etc. 
It  is  also  sometimes  the  seat  of  primary  neuritis. 

Paralysis  of  the  I?iternal  Popliteal  Nerve  causes  loss  of 
power  in  the  posterior  tibial  group  of  muscles  (includ- 
ing the  tibialis  posticus  and  popliteus)  and  the  long 
flexors  of  the  toes,  and  in  the  muscles  of  the  sole  of  the 
foot.  Extension  of  the  ankle-joint  is  impossible,  and  if 
the  branch  to  the  popliteus  is  involved  there  is  loss  of 
inward  rotation  of  the  leg  when  it  is  flexed.  When  the 
damage  to  the  nerve  is  sufficiently  severe  to  cause  anaes- 
thesia there  is  loss  of  sensation  over  the  outer  part  and 
posterior  aspect  of  the  lower  part  of  the  leg  and  on  the 
sole  of  the  foot.  The  posterior  tibial  nerve  is  rarely 
injured  except  in  fractures  of  both  bones  of  the  leg. 

The  branches  of  the  internal  popliteal  nerve,  the  ex- 
ternal and  internal  plantar  nerves,  are  rarely  involved 
alone. 

Paralysis  of  the  Exter?tal  Plantar  Nerve  causes  loss  of 


THE  DIAGNOSIS   OF  CLINICAL  TYPES.  533 

power  in  the  muscles  of  the  little  toe,  the  flexor  acces- 
sorius,  the  interossei,  the  two  outer  lumbricales,  and  the 
adductor  of  the  big  toe.  Certain  of  these  muscles  (lum- 
bricales and  interossei,  abductor  and  flexor  minimi  digiti) 
flex  the  first  phalanges,  and  extend  the  second  and  third, 
an  action  of  much  importance  in  walking,  in  the  propul- 
sion of  the  body  forward  just  before  the  foot  leaves  the 
ground.  The  loss  of  this  action  is  a  hindrance  in  walk- 
ing, as  is  the  later  contracture  of  the  opponents  of  the 
interossei,  which  leads  to  flexion  of  the  second  and  third 
phalanges.  The  sensory  loss  in  cases  of  external  plantar 
paralysis  includes  the  skin  of  the  outer  half  of  the  sole 
of  the  foot  and  of  the  little  toe,  and  that  of  the  adjacent 
half  of  the  fourth  toe. 

Paralysis  of  the  Internal  Plantar  Nerve  causes  loss  of 
power  in  the  short  flexor  of  the  toes,  the  intrinsic 
muscles  of  the  big  toe  (with  the  exception  of  the  adduc- 
tor), and  of  the  inner  lumbricales.  It  gives  rise  also  to 
anaesthesia  on  the  inner  part  of  the  sole  of  the  foot  and 
the  plantar  surface  of  the  three  inner  toes  and  the 
adjacent  half  of  the  fourth  toe. 

Paralysis  of  the  Small  Sciatic  Nerve  causes  paralysis  of 
the  gluteus  maximus,  with  consequent  interference  with 
the  power  of  rising  from  a  seat  and  loss  of  sensibility  in  an 
area  of  variable  size  on  the  posterior  surface  of  the  thigh. 

The  small  sciatic  nerve  is  damaged  only  in  disease  of 
the  sacral  plexus,  and  is  seldom  the  only  nerve  involved. 

The  Lumbar  Plexus  itself  may  be  involved  by  abdom- 
inal tumors,  enlarged  nodes,  or  psoas  abscess  ;  and  caries 
of  the  lumbar  spine  may  cause  compression  of  the  nerve- 
roots  that  make  up  the  plexus.  The  plexus  is  usually 
irregularly  invaded,  some  nerves  suffering  more  than 
others.  Sensory  symptoms  of  an  irritative  character  are 
often  among  the  first  symptoms  of  disease  of  the  plexus. 
There  is   frequently  severe  pain   in  the    course   of  the 


534         DISEASES   OF   THE   NERVOUS  SYSTEM. 

genito-crural,  ilio-inguinal,  and  ilio-hypogastric  nerves. 
Later  there  may  be  anaesthesia  of  irregular  distribution 
and  loss  of  power  in  the  distribution  of  the  obturatoi 
and  anterior  crural  nerves. 

The  Sacral  Plexus  is  liable  to  suffer  from  various 
forms  of  pelvic  disease,  especially  pelvic  tumors  and 
pelvic  inflammation.  Occasionally  it  is  compressed 
during  delivery.  Sometimes,  also,  it  is  the  seat  of 
primary  neuritis.  In  other  cases  it  is  the  seat  of  neuritis 
consequent  upon  extension  of  inflammation  from  the 
sciatic  nerve.  The  symptoms  of  disease  of  the  sacral 
plexus  are  usually  at  first  irritative  in  character  (pain, 
parsesthesia,  etc.);  later  they  are  indicative  of  a  destruc- 
tive process  (anaesthesia,  paralysis,  atrophy,  etc.). 

The  precise  distribution  of  these  symptoms  varies  in 
different  cases,  and  the  various  muscular  and  sensory  dis- 
tributions of  the  different  nerves  arising  from  the  plexus 
may  be  variously  and  unequally  affected.  The  manifes- 
tations of  disease  of  the  plexuses  are  rarely  confined  to 
the  distribution  of  any  single  nerve  arising  from  them, 
although  a  single  nerve  (as  the  anterior  crural)  may  for  a 
time  be  the  chief  or  exclusive  seat  of  the  symptoms. 
Plexus  disease  is  almost  invariably  unilateral,  but  in  rare 
cases  of  pressure  paralysis  and  spontaneous  neuritis  it  is 
bilateral.  The  distinction  of  lesions  of  the  lumbar  and 
sacral  plexuses  from  other  forms  of  disease,  especially 
cauda-equina  lesions  and  certain  forms  of  non-symp- 
tomatic neuralgia,  is  considered  elsewhere.  In  all  cases 
where  plexus  disease  is  suspected  a  careful  rectal  explo- 
ration is  of  the  utmost  importance  and  may  reveal  the 
presence  of  a  pelvic  tumor,  an  aneurism,  or  an  abscess 
which  exerts  pressure  upon  the  lumbar  or  sacral  plexus. 

Tumors  of  Peripheral  Nerves. — The  chief  forms 
of    tumors    of    peripheral    nerves    have    been    already 


THE   DIAGNOSIS    OF   CLINICAL   TYPES.  535 

mentioned  (see  278).  The  diagnosis  of  a  neuroma 
can  be  made  with  certainty  only  when  the  tumor  can  be 
felt.  The  presence  of  such  a  tumor  may,  however,  be 
suspected  in  cases  where  pain,  paraesthesia,  anaesthesia, 
and  loss  of  power  come  on  slowly  and  grow  progres- 
sively worse,  and  are  limited  to  the  distribution  of  one 
nerve-trunk.  But  there  is  no  way  of  distinguishing, 
purely  by  the  symptoms,  the  effects  of  damage  by  a  neu- 
roma from  the  effects  of  pressure  from  an  adjacent  nerve, 
or  even  from  the  effects  of  neuritis.  When  the  neuroma 
can  be  felt  there  arises  the  question  whether  it  is  a 
"  false  "  or  a  "  true  "  neuroma.  If  there  are  multiple 
tumors  they  are  probably  of  the  ''  true  "  form.  False 
neuromata  are,  however,  sometimes  multiple,  but  in  such 
cases  they  are  generally  of  rapid  growth.  If  the  tumor 
appears  to  grow  from  the  side  of  the  nerve  it  is  probably 
a  "  false  "  neuroma. 

The  symptoms  that  characterize  Lesions  of  the 
Cauda  Equina  in  general  have  been  elsewhere  touched 
upon  (p.  251). 

There  remain  for  consideration  here  certain  clinical 
forms  of  Cauda  disease  dependent  on  the  nature  of  the 
lesion — namely,  compression  and  crush.  Little  need  be 
said  here  regarding  crush  of  the  cauda  equina.  It  de- 
pends on  injury  from  fracture  and  dislocation,  usually 
of  the  upper  lumbar  vertebrae.  The  symptoms,  which 
vary  in  severity  in  different  cases,  are  of  immediate  on- 
set, and  the  nature  and  position  of  the  surgical  affection 
renders  the  localization  of  the  damage  perfectly  evident. 
The  question  which  arises  in  some  of  these  cases  as  to 
the  implication  of  the  conus  medullaris  has  already  been 
discussed.  Compression  of  the  cauda  may  be  of  rapid 
or  slow  development.  When  of  rapid  development  it 
always    depends    on    injury  —  usually    an    injury    which 


53^        DISEASES   OF  THE   NERVOUS   SYSTEM. 

causes  fracture  -  dislocation  of  lumbar  vertebrae.  In 
such  cases  there  may  be  both  crush  and  compression  of 
the  Cauda,  and  it  is  impossible  to  distinguish  between 
these  conditions.  It  is  probable  that  in  rare  cases  the 
Cauda  is  rapidly  compressed  by  hemorrhage  in  the  ab- 
sence of  fracture-dislocation.  When  the  compression  of 
the  Cauda  is  slow,  the  diagnosis  of  the  condition  causing 
it  is  more  difficult  than  in  surgical  cases,  as  all  external 
indications  are  wanting.  The  only  exception  to  this  is 
where  the  compression  depends  on  the  pressure  of  a 
meningocele  in  spina  bifida,  the  nature  of  the  case  being 
here  sufficiently  obtrusive.  Slow  compression  of  the 
Cauda  usually  depends  on  tumor  within  the  spine.  The 
symptoms  differ  considerably  in  different  cases  of  tumor, 
and  the  number  of  cases  that  have  been  carefully  studied 
is  not  yet  sufficient  to  enable  us  to  draw  conclusions 
which  fit  all  cases.  The  following  may  be  regarded  as  the 
chief  clinical  characters  of  tumor  of  the  cauda  equina  : 

1.  Severe  pain  in  the  region  of  the  sacrum,  persistent 
and  increasing  in  intensity.  Often  the  pain  radiates 
down  the  back  of  the  legs.  The  sacrum  may  be  tender 
to  pressure  in  the  median  line,  and  the  spontaneous  pain 
may  be  greatly  increased  during  movement.  This  sacral 
pain  is  usually  the  first  symptom  of  a  cauda  tumor.  It 
may  continue  or  pass  away  when  anaesthesia  is  de- 
veloped. 

2.  The  gradual  development  of  anaesthesia  of  the 
peculiar  distribution  already  described  (p.  253),  loss  of 
control  over  the  bladder  (often  very  early)  and  rectum, 
gradual  development  of  paralysis  and  atrophy  in  the 
legs,  especially  below  the  knee,  and  gradual  but  early 
loss  of  knee-jerks,  perhaps  first  on  one  side.  Some- 
times there  are  attacks  of  clonic  spasm  in  the  muscles  of 
the  legs. 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.  537 

3.  The  symptoms  are  always  bilateral  and  are  gen- 
erally highly  symmetrical. 

The  accurate  localization  of  the  lesion  in  the  cauda 
depends  on  a  knowledge  of  the  representation  of  various 
sensory  and  motor  structures  in  the  cauda,  but  an  accu- 
rate diagnosis  is  sometimes  impossible.  The  diagnosis  of 
the  nature  of  the  tumor  is  usually  impossible.  When  it 
is  made  it  is  upon  general  principles.  Syphiloma,  sar- 
coma, and  cavernous  angioma  have  been  met  with. 
Most  cases  of  tumor  of  the  cauda  equina  are  progressive 
(one  to  three  years),  but  in  rare  cases,  apparently  belong- 
ing to  this  category,  they  have  retrogressed,  or  remained 
for  a  long  time  stationary. 

The  points  of  distinction  between  tumor  of  the  cauda 
equina  and  tumor  of  the  spinal  cord  do  not  require  special 
mention.  They  are  sufficiently  covered  by  the  points  of 
difference  between  cauda  and  cord  lesions  that  have  been 
touched  on  elsewhere  (see  Localization).  There  is, however, 
one  disease  of  the  cord  which  is  liable  to  be  confounded 
with  a  tumor  of  the  cauda  equina,  namely,  locomotor 
ataxia.  Sharp  radiating  pains,  paraesthesia,  involvement  of 
the  bladder,  loss  of  knee-jerks,  and  impaired  gait  are  com- 
mon to  both.  But  in  locomotor  ataxia  the  pains  are  incon- 
stant, there  is  distinct  ataxia,  and  pupillary  symptoms  are 
usually  present  early.  The  absence  of  ataxia  and  pupillary 
symptoms,  and  the  presence  of  marked  atrophy  and  dis- 
tinctive anaesthesia,  are  sufficient  to  prevent  error  if  the 
possibility  of  confounding  the  conditions  is  remembered. 
There  is  usually  no  difficulty  in  distinguishing  a  tumor  of 
the  cauda  from  disease  of  the  limb  plexuses.  In  disease 
of  the  plexuses  the  symptoms  are  generally  one-sided. 
Anaesthesia,  if  present,  is  of  irregular  distribution. 
Tumor  of  the  cauda  equina,  however,  generally  causes 
bilateral  symptoms  and  the  peculiar  areas  of  anaesthesia 


538  DISEASES   OF   THE   NERVOUS   SYSTEM. 

SO  often  mentioned.  A  rectal  examination  will  sometimes 
clear  up  the  diagnosis.  Bilateral  lumbo-sacral  neuritis  of 
primary  origin  may  for  some  time  cause  symptoms  that 
cannot  be  distinguished  from  a  commencing  cauda 
lesion.  On  the  other  hand,  the  symptoms  of  tumor  may 
be  for  a  time  unilateral.  In  such  cases  it  is  necessary  to 
wait  for  unequivocal  symptoms  to  appear. 

Multiple  Neuritis  (Polyneuritis — Disseminated  Neu- 
ritis).— The  term  ''  multiple  neuritis  "  is  used  to  designate 
a  large  and  important  class  of  cases  in  which  several 
nerves  become  inflamed  either  at  the  same  time  or  in 
quick  succession.  Broadly  speaking,  these  cases  resemble 
one  another  in  the  occurrence  of  motor,  sensory,  and 
trophic  disturbances,  but  they  differ  so  much  in  the 
degree,  distribution,  and  course  of  their  symptoms  that  it 
would  not  be  profitable  to  study  them  as  a  single  group. 
All  the  plans  yet  proposed  for  classifying  cases  of  multiple 
neuritis  are  imperfect.  Perhaps  the  least  objection- 
able classification  is  that  based  on  etiology  (toxic  form, 
infectious  form,  spontaneous  form,  etc.).  For  the  present 
purpose,  however,  it  is  impracticable  to  adhere  to  any  one 
classification  ;  it  is  preferable  to  study  separately  in  their 
diagnostic  relations  the  chief  clinical  types  of  multiple 
neuritis  as  they  occur  in  practice.  We  may  thus  dis- 
tinguish the  following  forms  of  neuritis:  (i)  alcoholic 
neuritis,  (2)  diphtheritic  neuritis,  (3)  neuritis  from  lead 
poisoning,  (4)  neuritis  from  carbonic  oxide  poisoning,  (5) 
Beriberi,  and  (6)  leprous  neuritis.'     To  these  varieties  of 

'  This  list  comprises  the  most  important  forms  of  multiple  neuritis. 
Many  other  kinds  of  neuritis  (dependent  on  different  causes)  might 
be  described,  but  most  of  these  are  not  sufficiently  distinctive  or  com- 
mon to  require  separate  discussion.  Some  of  them  will,  however,  be 
touched  on  in  connection  with  the  diagnosis  of  the  forms  above 
enumerated. 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.  539 

neuritis  may  be  added  a  condition  whose  pathology  is  as 
yet  unsettled,  but  which  probably  depends  on  multiple 
neuritis — acute  ascending  paralysis. 

Alcoholic  Neuritis. — The  diagnosis  of  alcoholic  multiple 
neuritis  is  based  chiefly  on  a  combination  of  motor 
symptoms  of  paraplegic  type  with  obtrusive  and  rather 
characteristic  sensory  symptoms,  the  onset  of  the  process 
being  subacute,  or,  as  is  less  often  the  case,  acute. 

I.  Sensory  Symptoms.  The  sensory  symptoms  of  alco- 
holic neuritis,  though  they  usually  develop  hand  in 
hand  with  motor  paralysis,  are  often  the  earliest  indication 
of  the  disease.  They  are  chiefly  irritative  in  character  and 
consist  at  first  of  paraesthesias — as  tingling,  sensations  of 
"pins  and  needles,"  rheumatoid  pains,  etc.,  in  the  ex- 
tremities— usually  the  lower  extremities,  sometimes  the 
arms.  These  symptoms  are  soon  succeeded  by  the  fol- 
lowing manifestations  : 

(i)  Pain,  sharp  or  burning,  rarely  dull,  in  the  nerve- 
trunks  of  the  affected  extremities  and  often  in  the  areas 
supplied  by  these  nerves.  The  pain  may  be  very  severe. 
Occasionally  it  is  slight. 

(2)  Hyperaesthesia  (hyperalgesia)  of  the  extremities. 

(3)  Muscular  tenderness.  The  muscles  when  pressed 
are  very  sensitive.  This  is  a  highly  characteristic  and 
common  symptom  of  alcoholic  neuritis. 

(4)  Anaesthesia,  partial  loss  of  muscular  sense  and  par- 
tial loss  of  pain  and  temperature  sense.  The  anaesthesia 
may  be  confined  to  irregular  areas  of  skin,  or  even  to  the 
distribution  of  a  single  nerve  (as  the  ulnar).  Generally 
it  implicates  a  considerable  part  of  the  distal  portion  of 
the  extremity. 

The  sensory  symptoms  of  multiple  neuritis  are  sym- 
metrically distributed,  the  degree  of  symmetry  being 
often  very  striking. 


540         DISEASES   OF   THE   NERVOUS   SYSTEM. 

II.  Motor  Symptoms. — Sensory  symptoms  are  not  long 
present  before  loss  of  power  becomes  associated  with 
them.  The  paralysis  usually  commences  in  the  legs  but 
may  begin  in  and  be  limited  to  the  arms.  Both  legs  are 
involved  together  or  in  rapid  succession.  The  weakness 
is  especially  marked  below  the  knees  but  usually  extends  to 
the  thigh  muscles.  Often  the  paralysis  extends  to  the 
upper  extremities — first  to  the  muscles  of  the  hand,  then 
to  the  forearm.  The  extensor  groups  of  muscles  are 
especially  affected  in  both  extremities,  but  often  both 
flexors  and  extensors  suffer  in  high  degree.     In  the  leg 


FIG.  65. 
Multiple  alcoholic  neuritis  ;  palsy  of  extensors  of  the  wrist  and  flexors  of  ankle.     (Gowers.) 

there  is  "drop-foot,"  in  the  upper  extremity  "wrist-drop." 
The  bilateral  drop-foot  is  as  suggestive  of  alcoholic  neu- 
ritis as  is  wrist-drop  of  lead  neuritis.  The  paralyzed 
muscles  are  flaccid,  become  much  atrophied,  and  show  the 
RD.  In  rare  cases  there  is  double  facial  paralysis.  Par- 
alysis of  the  sphincters  is  very  rare,  unless  there  is  also 
myelitis. 

Associated  with  these  motor  and  sensory  phenomena 
are  often  the  following  conditions  : 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.  541 

(  i)  Inco-ordination,  usually  slight  in  degree  and  con- 
fined to  the  lower  extremities.  Occasionally  the  inco- 
ordination is  the  most  obtrusive  symptom  of  the  disease, 
being  greatly  out  of  proportion  to  the  sensory  and  para- 
lytic phenomena.  Such  cases  may  closely  resemble  loco- 
motor ataxia,  and  are  hence  termed  "pseudo-tabes." 

( 2 )  Loss  of  myotatic  irritability  in  the  paralytic 
muscles.  In  the  cases  where  the  lower  extremities  are 
affected,  the  knee-jerk  is  lost  early,  even  when  there  is 
only  slight  loss  of  power  in  the  extensors  of  the  knee. 
Cases  occasionally  occur,  however,  in  which  the  knee- 
jerk  is  not  lost  at  any  time  in  the  disease,  probably 
because  in  these  cases  the  extensors  of  the  knee  are  not 
involved. 

(3)  Cerebral  symptoms  are  seldom  wanting  in  severe 
cases  of  multiple  neuritis,  and  are  especially  constant  in 
women.  They  comprise  active  delirium,  with  illusions 
and  hallucinations,  insomnia,  loss  of  memory,  fabrica- 
tions, and  general  mental  failure  constituting  a  distinct 
psychosis,  which  may  accompany  polyneuritis  (Korssa- 
kow's  disease).  These  symptoms  are  not  usually  present 
until  the  disease  is  well  established.  They  may,  how- 
ever, be  present  from  the  first,  as  when  multiple  neuritis 
develops  during  delirium  tremens. 

(4)  Trophic  symptoms  in  the  skin  and  nails  of  the 
paralyzed  extremities  are  common,  and  resemble  those 
observed  in  simple  neuritis. 

When  the  onset  of  the  disease  is  acute,  there  may  be 
considerable  elevation  of  temperature  during  the  first 
weeks  of  the  disease.  The  duration  of  the  disease  varies 
with  the  acuteness  and  severity  of  the  process.  In  a 
moderately  severe  case  of  subacute  development  (/.  <?., 
a  typical  case  as  regards  course )  the  severity  of  the 
symptoms  increases  during  a  month  or  six  weeks,  and 


542  DISEASES  OF   THE   NERVOUS   SYSTEM. 

improvement  in  power  does  not  begin  until  a  month  or 
six  weeks  more  have  elapsed.  Some  chronic  cases  run  a 
very  long  and  tedious  course  ( one  to  two  years  ).  Ex- 
cept in  mild  cases,  contractures  are  apt  to  remain  over. 

The  etiology  of  cases  of  alcoholic  neuritis  is  an  aid  in 
the  diagnosis  of  the  condition,  since  a  history  of  alco- 
holic excess  is  seldom  wanting  ( vide  p.  293).  Such  a 
history  is,  however,  not  often  necessary  for  a  diagnosis  ; 
the  distribution  of  the  palsy,  the  obtrusive  and  suggestive 
sensory  symptoms  and  the  escape  of  the  sphincters  suffice 
to  indicate  the  nature  of  the  case.  But  the  diagnosis  of  the 
condition  is  not  always  so  simple.  There  are  three  con- 
ditions with  which  the  disease  is  readily  confounded. 
These  are  poliomyelitis,  transverse  myelitis,  and  locomotor 
ataxia. 

Paralysis,  muscular  atrophy,  RD,  and  loss  of  tendon 
reflex  occur  both  in  alcoholic  neuritis  and  in  poliomyelitis. 
In  the  latter  condition,  however,  sensory  symptoms  are 
absent  (  except,  perhaps,  during  the  onset  of  the  symp- 
toms ),  the  paralysis  is  unsymmetrical,  if  not  unilateral ; 
there  is  some  retrogression  of  the  paralysis  after  the 
onset,  especially  if  this  be  acute,  and  the  development  of 
the  symptoms  is  fairly  rapid  if  not  acute.  In  alcoholic 
neuritis,  on  the  other  hand,  sensory  symptoms  are  obtru- 
sive, the  paralysis  is  usually  symmetrical  and  always 
progressive,  and  the  onset  is  usually  ( though  not  always ) 
gradual. 

The  resemblance  between  some  cases  of  alcoholic 
neuritis  and  locomotor  ataxia  is  close.  In  both  condi- 
tions there  may  be  inco-ordination,  loss  of  knee-jerks, 
sharp  pains  in  the  lower  extremities,  defective  muscular 
sense,  and  great  unsteadiness  when  the  eyes  are  closed 
and  the  feet  are  close  together  (  Romberg's  symptom). 
The  chief  diagnostic  points  are  the  following  :     In  alco- 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.  543 

holic  neuritis  there  are  no  true  lightning  pains,  the  mus- 
cles are  tender  to  pressure,  there  is  distinct  loss  of  power, 
atrophy  and  some  degree  of  RD,  bladder  symptoms  are 
absent,  and  the  inco-ordination,  if  sufficiently  marked  to  be 
confounded  with  that  of  locomotor  ataxia,  is  distinguished 
by  its  rapid  development  in  the  early  course  of  the  disease. 

An  occasional  source  of  difficulty  in  diagnosis  arises 
from  the  circumstance  that  locomotor  ataxia  may  be 
complicated  with  severe  neuritis.  Whenever  unequivocal 
symptoms  of  locomotor  ataxia  are  associated  with  paral- 
ysis and  muscular  atrophy  of  limited  extent,  or  with 
limited  patches  of  anaesthesia  and  analgesia,  it  is  safe  to 
conclude  that  those  symptoms  depend  on  neuritis.^  But 
cases  occur  in  which  localized  sensory  and  motor  dis- 
turbances are  associated  with  symptoms  that  strongly 
suggest  locomotor  ataxia,  but  are  nevertheless  equivocal. 
The  question  arises  in  such  instances  :  have  we  to  deal 
with  a  case  of  alcoholic  multiple  neuritis,  or  with  a  case 
of  locomotor  ataxia,  associated  with  severe  neuritis  ?  If 
this  question  cannot  be  decided  by  means  of  the  indi- 
cations that  have  been  already  mentioned,  it  may  be 
necessary  to  wait  and  watch  the  course  of  the  symptoms 
before  reaching  a  conclusion. 

There  is  seldom  any  reason  for  confounding  alcoholic 
neuritis  and  transverse  myelitis.  In  myelitis  involving 
the  lumbar  enlargement  there  is  paralysis  of  motion 
and  sensation  in  the  lower  extremities  and  loss  of  knee- 
jerks.  But  the  motor  paralysis  in  such  cases  shows  no 
tendency  to  remain  confined  to  the  distal  portion  of 
the  extremities  ;  the  sensory  symptoms  differ  from  those 
of  alcoholic  neuritis  in  that  they  are  largely  indicative 

^  The  gastric  and  laryngeal  crises  of  tabes  probably  depend  on 
neuritis,  but,  of  course,  their  occurrence  gives  rise  to  no  question  as 
to  diagnosis. 


544         DISEASES   OF   THE  NERVOUS   SYSTEM. 

of  destruction  of  nerve  elements  rather  than  irritation  ; 
the  sphincters  are  affected,  and  often  there  is  a  girdle- 
pain.  In  myelitis  above  the  lumbar  enlargement  the 
knee-jerks  are  not  lost,  but  are  increased,^  and  this  fea- 
ture alone  serves  to  distinguish  it  from  a  neuritis  involv- 
ing exclusively  the  lower  extremities. 

In  rare  instances  alcoholic  neuritis  is  complicated  by 
myelitis,  and  the  bearing  of  such  an  occurrence  upon 
prognosis  renders  its  recognition  exceedingly  important. 
The  following  facts  are  to  be  borne  in  mind  in  consid- 
ering the  possible  existence  of  a  complicating  myelitis. 

During  the  time  when  a  case  of  alcoholic  neuritis  is 
increasing  in  severity  we  cannot  say  positively  that  the 
lesion  will  not  extend  to  the  cord,  and  the  question  of 
exact  localization  can  hardly  be  said  to  have  arisen. 
When,  however,  the  symptoms  become  stationary,  the 
question  may  come  up.  If  there  is  no  improvement  in 
the  symptoms  after  they  have  remained  stationary  for  a 
period  of  four  months,  it  is  highly  probable  that  the  cord 
is  involved,  or  that  the  patient  is  still  taking  alcohol. 
Again,  if  additional  symptoms  make  their  appearance 
after  the  neuritic  process  has  been  stationary  for  a  time, 
such  a  progression  probably  depends  on  myelitis,  pro- 
vided the  continued  use  of  alcohol  can  be  excluded. 
The  symptoms  which  under  these  circumstances  are  par- 
ticularly significant  are  an  increase  of  paralysis,  rapid 
muscular  atrophy,  the  replacement  of  paraesthesia  by 
anaesthesia,  loss  of  control  over  the  sphincters,  and  the 
appearance  of  bedsores. 

The  relation  of  alcoholic  neuritis  to  the  condition 
known  as  acute  ascending  paralysis  is  discussed  in  con- 
nection with  the  latter  disease. 

'  In  rare  cases  of  acute  myelitis  above  the  lumbar  enlargement 
the  knee-jerks  are  temporarily  lost. 


THE    DIAGNOSIS   OF   CLINICAL  TYPES.         545 

Cases  are  not  rarely  met  with  in  which  there  are  numb 
ness,  tingling,  pain,  and  slight  anaesthesia  in  irregular 
areas  of  the  hands  (acroparesthesia).  These  cases  occur 
usually  in  women  about  the  time  of  the  climacteric,  espe- 
cially in  those  whose  general  health  is  for  some  reason 
depressed,  and  whose  hands  are  much  exposed  to  the 
action  of  water.  The  patients  are  very  commonly  per- 
sons who  do  not  use  alcohol  to  excess.  It  is  only  neces. 
sary  to  be  aware  of  the  occurrence  of  this  affection, 
which  depends  probably  on  a  palmar  neuritis,  to  avoid 
confusing  it  with  the  early  stage  of  alcoholic  neuritis. 

Lead-Neuritis. — The  chief  symptoms  of  neuritis  from 
lead  are  localized  muscular  paralysis  and  atrophy  and 
pains  in  the  limbs.  These  conditions  may  be  associated, 
or  may  occur  separately.  The  most  important  and  char- 
acteristic result  of  lead  neuritis  is  the  local  paralysis. 
Generally  the  paralysis  affects  the  extensor  muscles  of 
the  wrist  and  fingers  and  causes  bilateral  wrist-drop,  a 
condition  highly  suggestive  of  lead  neuritis.  Usually 
the  paralysis  remains  confined  to  the  upper  extremities, 
but  it  sometimes  involves  the  muscles  of  the  legs,  espe- 
cially the  long  extensors  of  the  toes  and  peronei.  In 
the  arm  the  deltoid  not  rarely  suffers,  and  may  suffer 
early.     The  biceps  is  also  occasionally  involved. 

A  peculiarity  of  considerable  diagnostic  importance 
relates  to  the  distribution  of  the  palsy  in  the  forearm 
muscles.  In  a  very  large  proportion  of  cases  of  lead  palsy 
two  muscles  of  the  forearm  are  exempt  from  the  loss  of 
power  ;  these  are  the  supinator  longus  and  the  extensor 
ossis  metacarpi  pollicis.  In  the  majority  of  cases  of 
lead  palsy  from  neuritis,  the  loss  of  power  precedes  the 
wasting  of  the  muscles,  and  the  muscles  present  the 
RD.  In  other  words,  the  character  of  the  palsy  closely 
resembles  that  observed  when  a  motor  nerve  has  been 


546         DISEASES   OF  THE  NERVOUS   SYSTEM. 

involved  in  a  traumatic  lesion.  But  the  type  of  lead 
paralysis  is  not  always  of  this  kind.  Cases  occur  in 
which  paralysis  and  atrophy  of  the  muscles  develop 
together,  pari  passu,  and  in  which  there  is  simply  a 
gradual  and  proportional  diminution  of  the  irritability 
of  the  muscles  to  the  faradic  and  galvanic  currents.  In 
these  cases  the  paralysis  may  begin  in  almost  any  part 
of  the  extremities,  but  it  is  especially  apt  to  begin  in  the 
small  muscles  of  the  hand.  This  form  of  local  muscu- 
lar atrophy  may  be  likened  to  that  which  is  so  character- 
istic of  progressive  muscular  atrophy. 

It  is  important  to  recognize  clearly  the  existence  of 
these  two  types  of  paralysis  from  lead,  for,  though  inter- 
mediate forms  occur,  the  large  majority  of  cases  conform 
to  one  or  other  type.  Moreover,  it  is  probable  that  the 
two  types  of  paralysis  are  referable  to  a  difference  in 
the  seat  of  the  lesion.  In  the  type  which  resembles  the 
paralysis  resulting  from  an  injury  of  a  peripheral  nerve, 
the  lesion  is  almost  always  confined  to  the  peripheral 
nerves  ;  in  the  type  which  resembles  progressive  muscu- 
lar atrophy,  there  is  often,  and  perhaps  always,  involve- 
ment of  the  ganglion-cells  of  the  anterior  horns  of  the 
spinal  cord  as  well. 

Sensory  symptoms  in  lead  paralysis  are  usually  slight, 
and  may  be  entirely  absent.  Sometimes  there  is  consid- 
erable pain  in  the  limbs  affected  at  the  time  of  the  onset 
of  the  symptoms.  Muscular  tenderness  may  be  found 
also.  Sometimes  there  is  slight  anaesthesia  of  the  skin 
over  the  affected  muscles.  In  cases  of  lead  poisoning 
without  paralysis  there  are  often  dull  or  sharp  limb 
pains,  dependent  on  slight  neuritis,  but  not  distinctive  in 
character.  The  reflexes  are  lost  in  lead  neuritis  under  the 
same  conditions  that  cause  their  loss  in  alcoholic  neuritis. 

The  diagnosis  of  lead  neuritis  is  usually  easy.     From 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.         S47 

alcoholic  neuritis  it  is  distinguished  by  the  localization 
of  the  paralysis  to  the  upper  extremities,  by  the  absence 
or  trifling  character  of  sensory  symptoms,  and  by  the  pres- 
ence of  other  indications  of  lead  poisoning,  such  as 
colic,  the  lead  line  on  the  gums,  and  anaemia.  Cases  of 
alcoholic  neuritis  occur,  however,  in  which  the  paralysis 
is  limited  to  the  upper  extremity,  and  in  which  the  sen- 
sory symptoms  are  slight.  In  such  a  case  the  chief 
points  of  distinction  from  lead  neuritis  are  the  involve- 
ment of  the  supinator  longus  and  extensor  ossis  meta- 
carpi  pollicis  and  a  distinct  history  of  alcoholic  excess. 
Sometimes  an  old-standing  case  of  lead  neuritis  comes 
under  observation  in  which  there  are  contractures  in  the 
arms  and  legs,  which  have  developed  after  slowly  pro- 
gressive paralyses  (including  wrist-drop  and  drop-foot), 
and  in  which  there  is  no  history  of  lead  poisoning. 
Unless  some  source  of  lead  poisoning  can  be  traced,  the 
nature  of  such  a  case  may  not  be  recognized. 

The  diagnosis  from  progressive  muscular  atrophy  may 
be  difficult  in  the  cases  already  mentioned,  which  resem- 
ble this  disease  in  the  nature  and  distribution  of  the 
palsy.  A  history  of  lead  poisoning  or  the  detection  of 
lead  in  the  urine  may  be  necessary  before  a  positive 
diagnosis  is  made. 

The  distinction  between  lead  neuritis  and  musculo- 
spiral  paralysis  has  been  already  considered  (see  p.  490). 

Arsenical  Neuritis. — The  symptoms  that  characterize 
arsenical  neuritis  resemble  both  those  of  alcoholic  neu- 
ritis and  those  of  lead  neuritis.  These  symptoms  are 
paralysis  of  the  muscles  of  the  limbs,  especially  of  the 
extensors  of  the  hand  and  feet,  and  inco-ordination, 
especially  in  the  lower  extremities.  With  these  symp- 
toms there  are  usually  marked  sensory  disturbances,  in- 
cluding severe  darting  pains  in  the  arms  and  legs  and 


548         DISEASES  OF  THE  NERVOUS   SYSTEM. 

anaesthesia  of  the  skin  over  the  affected  muscles.  The 
knee-jerks  are  generally  lost. 

The  chief  points  of  distinction  between  arsenical  and 
lead  neuritis  are  the  usual  onset  of  the  former  after 
acute  arsenical  poisoning,  the  greater  severity  of  the 
sensory  symptoms,  and  the  involvement  of  the  anterior 
tibial  and  peroneal  groups  of  muscles  in  the  leg  in 
addition  to  the  extensor  paralysis  in  the  upper  extremities. 

In  the  cases  that  depend  on  chronic  arsenic  poisoning 
(as  from  the  careless  use  of  medicinal  preparations  of 
arsenic),  the  cause  of  the  neuritis  is  usually  sufficiently 
evident.  Where  there  is  some  doubt  as  to  the  nature  of 
the  case  the  presence  of  arsenic  in  the  urine  may  deter- 
mine the  diagnosis.  The  distinction  of  arsenical  from 
alcoholic  neuritis  may  be  very  difficult  in  the  absence  of 
a  history  of  alcoholic  excess.  Here,  again,  the  finding  of 
arsenic  in  the  urine  may  clear  up  the  nature  of  the  case. 

Neuritis  from  Carbonic  Oxide  Poisoning. — This  is  a 
rare  affection,  the  symptoms  of  which  vary  widely  in 
different  cases.  In  most  cases  there  are  obtrusive  sen- 
sory and  motor  symptoms,  and  in  many  cases  vaso- 
motor and  trophic  symptoms  are  also  present.  The 
sensory  symptoms  of  carbonic  oxide  neuritis  are  numb- 
ness, partial  loss  of  tactile  sensibility  and  sometimes 
pain  in  the  extremities — usually  over  the  muscles 
that  are  the  seat  of  paralysis.  The  motor  symptoms 
consist  of  local  paralyses  of  irregular  and  variable  dis- 
tribution. In  some  cases  the  paralysis  has  the  distribu- 
tion so  often  observed  in  alcoholic  neuritis,  causing 
double  wrist-drop  and  drop-foot.  Sometimes  the  paraly- 
sis is  confined  to  a  single  nerve  territory  (ulnar,  radial 
or  peroneal  paralysis).*     The  paralysis  has  been  known 

'  There  is  some  reason  to  think  that  the  paralysis  in  some  of  these 
cases  was  due  to  pressure  on  a  nerve-trunk  during  the  period  of  un- 
consciousness which  usually  preceded  the  development  of  the  neuritis. 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.  549 

to  be  bemiplegic  in  distribution.  In  other  cases  only 
the  lower  extremities  have  been  involved.  In  one  case 
all  the  muscles  of  the  eyeball,  intrinsic  and  extrinsic, 
were  paralyzed.  The  vaso-motor  and  trophic  symptoms 
of  carbonic  oxide  neuritis  include  redness  of  the  skin, 
oedema,  changes  in  surface  temperature  and  herpetic 
eruptions   along  the   course  of  nerve-trunks. 

The  recognition  of  carbonic  oxide  neuritis  is  usually 
easy,  because  there  is  generally  a  distinct  history  of 
exposure  to  the  gas,  which  is  developed  in  considerable 
quantities  whenever  coal  or  charcoal  is  burned  in  a 
space  to  which  oxygen  has  imperfect  access.  In  cities 
a  common  mode  of  poisoning  by  carbonic  oxide  gas  is 
the  inhalation  of  illuminating  gas  which  has  escaped 
into  a  closed  room.  A  period  of  linconsciousness  usually 
precedes  by  a  few  hours  or  days  the  symptoms  of  neu- 
ritis, but  the  loss  of  consciousness  may  be  partial,  and 
is  sometimes  entirely  absent.  The  neuritic  symptoms 
are  often  preceded  or  accompanied  with  pain  in  the 
hypocondriac  region,  shortness  of  breath,  and  dyspnoea 
on  exertion.  Transient  mental  symptoms,  such  as  de- 
pression of  spirits  and  loss  of  memory,  are  of  common 
occurrence  in  the  early  stage  of  the  neuritic  affection, 
and  are  rather  characteristic.  These  symptoms  may 
persist  for  many  months. 

Diphtheritic  Neuritis. — The  symptoms  that  indicate  the 
presence  of  diphtheritic  neuritis  are  usually  highly  char- 
acteristic. They  consist  chiefly  of  motor  phenomena  of 
peculiar  distribution.  The  paralysis  is  of  gradual  onset 
and  development  in  each  part  and  usually  involves  in 
succession  different  and  widely  separated  regions,  so  that 
recovery  of  power  often  goes  on  in  the  parts  originally 
affected  while  the  paralysis  is  invading  other  regions. 
The  order  in  which  the  paralysis  involves  the  affected 


550        DISEASES   OF   THE   NERVOUS   SYSTEM. 

parts  varies  in  different  cases.  The  paralysis  usually  be- 
gins in  the  palate,  the  loss  of  power  being  shown  by  the 
nasal  tone  of  the  voice  and  the  partial  regurgitation  of 
food.  The  paralysis  may  not  spread  to  other  parts,  but 
usually  it  soon  involves  the  ciliary  muscle  of  the  eye 
and  gives  rise  to  loss  of  power  of  accommodation,  with 
impaired  vision  for  near  objects.  Very  often  at  the  time 
when  accommodation  is  first  impaired  the  loss  of  power 
extends  to  the  limbs.  The  legs  are  usually  involved  be- 
fore and  in  greater  degree  than  the  arm.  The  paralysis 
is  generally  slight  in  degree  and  always  bilateral.  It  is 
always  of  the  atonic  kind,  the  muscles  being  flabby  and 
relaxed. 

With  these  characteristic  symptoms  there  is  associated 
a  symptom  which  is  so  constant  as  to  be  of  much  diag- 
nostic value.  This  is  loss  of  knee-jerk.  The  loss  occurs 
early  in  the  disease,  and  is  generally  present  even  when 
the  legs  are  not  paralyzed. 

In  severe  cases  of  diphtheritic  neuritis  there  are  evi- 
dences of  implication  of  the  vagus — initial  retardation  of 
the  pulse  followed  by  irregular  and  rapid  heart  action. 
These  symptoms  have  little  diagnostic  value,  as  more 
characteristic  evidences  of  the  disease  usually  precede 
them  by  a  considerable  time. 

The  sensory  symptoms  of  diphtheritic  neuritis  are  gen- 
erally slight.  Sometimes  there  are  numbness,  tingling, 
hyperaesthesia,  and  anaesthesia  of  the  skin,  usually  at  the 
extremities  of  the  limbs  that  are  the  seat  of  paralysis. 

The  development  of  paralysis  of  the  palate  and  later  of 
paralysis  of  accommodation  and  progressive  weakness  of 
muscles  of  the  lower  extremities  constitute  so  distinctive 
a  group  of  symptoms  that  their  nature  is  always  clear. 
There  is,  moreover,  almost  invariably  the  history  of  a 
throat  affection  not  longer  than  a  month  before  the  onset 


THE   DIAGNOSIS   OF   CLINICAL   TYPES.  55 1 

of  neuritic  symptoms,  and  such  a  history  removes  any 
doubt  as  to  the  character  of  the  affection.  The  diagnosis 
may  be  more  difficult  when  the  local  evidences  of  diph- 
theria have  been  slight  and  the  palate  and  eye  symptoms 
have  been  slight  and  of  transient  duration.  Any  leg 
symptoms  which  exist  in  such  a  case  may  then  appear  to 
indicate  disease  of  the  spinal  cord.  The  presence  of 
ataxia  and  loss  of  knee-jerk  may  suggest  locomotor 
ataxia,  but  the  development  of  these  symptoms  is  too 
rapid,  and  there  is  too  little  pain  and  too  much  weakness 
in  the  legs  to  permit  an  error  to  be  made.  From  acute 
poliomyelitis  diphtheritic  neuritis  is  distinguished  by  the 
slower  onset,  the  marked  symmetry  and  slighter  degree 
of  the  paralysis  and  atrophy,  the  slighter  changes  in  the 
electrical  irritability  of  the  muscles,  and  the  presence  of 
sensory  symptoms. 

Beri-beri^  Kak-ke ^-^Th.Qst  names  are  applied  to  cases, 
apparently  of  multiple  neuritis,  of  widely  varying  severity 
and  type,  which  occur  in  endemic  or  epidemic  form 
along  the  coasts  of  Japan,  Borneo,  Ceylon,  India,  on  the 
coast  of  Brazil,  and  along  the  Red  Sea.  Cases  of  the 
disease  are  occasionally  seen  in  the  United  States,  chiefly 
in  Malayan  and  Chinese  sailors  or  in  travellers.  The 
condition  requires  only  brief  notice  here. 

The  chief  nervous  symptoms  of  beri-beri  are  pains  in 
the  extremities,  numbness,  tingling,  hyperaesthesia,  and 
anaesthesia,  associated  with  paralysis  and  muscular 
atrophy,  chiefly  of  the  lower  extremities,  but  sometimes 

'  There  is  still  considerable  question  as  to  the  cause  of  beri-beri. 
At  present  the  most  generally  accepted  view  is  that  it  is  a  contagious 
disease  dependent  on  the  entrance  into  the  body,  probably  by  the 
lungs  or  stomach,  of  a  specific  micro-organism.  There  are  many 
facts  which  suggest  that  the  disease  may  arise  from  an  animal 
poison,  which  occurs  in  decomposed  tunny-fish  or  in  bad  rice. 


552         DISEASES   OF   THE   NERVOUS   SYSTEM. 

of  the  extensors  of  the  forearm  as  well.  In  mild  cases 
the  development  of  these  symptoms  is  gradual,  and  re- 
covery occurs  usually  in  less  than  a  month.  In  severe 
cases  the  symptoms  are  of  rapid  onset  and  soon  reach  a 
high  degree  of  development.  In  some  cases  the  nervous 
symptoms  are  most  conspicuous,  but  in  the  majority  of 
cases  the  disease  is  of  the  "  hydropic  "  or  "  wet  "  type,  in 
which  the  nervous  symptoms  are  inconspicuous  and  a 
high  degree  of  general  oedema,  serous  effusion  into  the 
pleural  and  peritoneal  cavities,  and  heart  failure  are  the 
chief  manifestations.  In  other  cases  still,  also  of  the 
severe  type,  very  marked  nervous  symptoms  are  associ- 
ated with  the  symptoms  which  characterize  the  hydropic 
type  and  suggest  a  morbid  blood-state.  Paralysis  of  the 
diaphragm,  probably  from  phrenic  neuritis,  is  an  early 
symptom  in  many  of  the  severe  cases  of  beri-beri. 

The  distinction  of  this  disease  from  other  forms  of  mul- 
tiple neuritis  is  usually  not  difficult  if  the  conditions  under 
which  it  occurs  are  known,  as  it  is  only  observed  in  the 
United  States  in  persons  who  have  recently  been  in  the 
countries  where  the  disease  is  epidemic* 

Leprous  Neuritis  (Anaesthetic  Leprosy). — This  condi- 
tion, which  was  formerly  observed  only  in  the  countries 
where  leprosy  prevails  (Sandwich  Islands,  India,  Nor- 
way), is  now  occasionally  met  with  in  the  United  States. 
The  chief  manifestations  of  leprous  neuritis  are  anaes- 
thesia, muscular  atrophy  and  trophic  changes,  especially 
marked  in  the  most  distal  parts  of  the  extremities  and 
of  very  gradual  development.  The  anaesthesia  is  pre- 
ceded almost  invariably  by  the  appearance  of  a  patch  of 
hyperaesthesia,  commonly  on  the  hand  or  foot.     In  these 

^  A  disease  resembling  closely  some  forms  of  beri-beri  has  been  ob- 
served in  Massachusetts  fishermen  who  have  returned  from  fishing 
trips,  during  which  they  have  been  on  a  diet  chiefly  of  fish. 


THE   DIAGNOSIS   OF   CLINICAL  TYPES.  553 

hyperaesthetic  areas  there  is  usually  more  or  less  spon- 
taneous pain  of  a  burning  character.  Very  gradually, 
usually  after  the  lapse  of  many  months,  the  hyperses- 
thesia  is  replaced  by  anaesthesia.  In  some  cases  the 
loss  of  sensibility  corresponds  closely  to  the  distribution 
of  one  or  more  nerve  trunks  ;  more  often  the  loss  does 
not  correspond  accurately  to  nerve  distribution.  When 
anaesthesia  is  established  there  is  usually  some  weakness 
and  atrophy  in  the  muscles  of  the  part  involved,  the 
flexors  of  the  hands  and  feet  become  the  seat  of  con- 
tractions, and  in  consequence  of  the  resulting  deform- 
ities the  patient  becomes  unable  to  use  his  hands  or  to 
walk.  Both  hands  and  both  feet  are  usually  thus  in- 
volved in  from  four  to  six  years  after  the  first  symptoms 
of  the  disease.  When  the  muscular  atrophy  is  advanced 
other  trophic  changes  make  their  apearance.  An  ulcer 
appears  usually  near  the  base  of  the  big  toe.  This  ulcer 
remains  small,  but  after  a  time  involves  the  joint  of  the 
toe.  Then  the  bones  of  the  toe  become  necrosed  and 
the  part  eventually  separates.  In  a  similar  manner  the 
fingers  and  the  remaining  toes  are  gradually  involved. 

.The  symptoms  that  have  been  described  characterize 
the  anaesthetic  form  of  leprosy.  Very  often  these  symp- 
toms are  associated  with  the  appearance  of  small  hard 
nodules  on  various  parts  of  the  body,  and  especially  the 
face,  and  with  fever  (so-called  "  tubercular  "  form  of  lep- 
rosy) a  combination  of  symptoms  known  as  the  "  mixed  " 
form  of  leprosy. 

The  distinction  of  anaesthetic  leprosy  from  syringo- 
myelia has  been  already  touched  upon  (p.  464). 

Acute  Ascending  Paralysis  (Landry's  Paralysis). — The 
designation  acute  ascending  paralysis  is  employed  both 
in  a  restricted  sense  and  in  a  more  general  sense.    In 


554        DISEASES   OF  THE   NERVOUS   SYSTEM. 

consequence  of  this  difference  in  usage  some  confusion 
has  arisen. 

Acute  ascending  paralysis,  in  the  restricted  sense,  is 
a  disease  characterized  by  :  (i)  the  rapid  development  of 
ascending  paralysis  (legs,  then  arms,  diaphragm,  neck, 
and  sometimes  palate)  with  flaccidity  of  the  muscles  in- 
volved ;  (2)  loss  of  reflex  action  (including  knee-jerks) 
in  the  muscles  paralyzed  ;  (3)  the  absence  of  fever  ; 
(4)  the  absence  of  a  considerable  degree  of  pain  or  sen- 
sory loss  ;  and  by  (5)  the  absence  of  muscular  atrophy 
and  RD  in  the  cases  which  live  long  enough  to  have 
made  the  development  of  these  conditions  possible.  As 
to  the  character  of  the  lesion  which  gives  rise  to  these 
symptoms,  it  is  sufficient  to  say  that  nothing  whatever  is 
at  present  known,  and  that  there  is  as  yet  no  sufficient 
reason  for  regarding  any  of  the  cases  of  this  type  as 
dependent  on  multiple  neuritis.' 

In  the  wider  sense  of  the  designation,  acute  ascending 
paralysis  includes,  in  addition  to  the  well  defined  group 
of  cases  just  mentioned,  cases  in  which  the  loss  of  motor 
power  has  the  same  rapid  development  and  ascending 
course  as  in  those  cases,  but  in  which  there  are  marked 
sensory  symptoms  (pain,  paraesthesia,  anaesthesia),  RD, 
muscular  atrophy,  and,  in  some  cases,  affections  of  the 
sphincters,  and  fever.^  There  is  good  reason  to  believe 
that  many  of  the  cases  which  belong  in  this  second  group 

'  There  is  some  reason  to  think  that  these  cases  may  depend  on  the 
action  of  a  toxic  substance  in  the  blood  upon  the  fibrillary  termina- 
tions of  the  upper  segment  of  the  motor  tract,  and  upon  the  motor 
ganglion-cells  of  the  cord  with  which  these  are. connected.  The  rela- 
tion of  some  cases  to  acute  specific  diseases,  and  the  enlargement  of 
the  spleen  and  lymph  nodes  sometimes  observed,  suggest  the  agency  of 
a  toxic  substance. 

'^  The  propriety  of  including  these  cases  under  Landry's  paralysis  is 
rather  doubtful,  but  has  been  unquestioned  by  some  writers  of  excel- 
lent repute. 


THE  DIAGNOSIS   OF  CLINICAL  TYPES.  555 

are  instances  of  multiple  neuritis,'  and  it  is  certainly 
true  that  there  occur  undoubted  cases  of  alcoholic  neu- 
ritis, diphtheritic  neuritis,  and  beri-beri,  in  which  the 
symptoms  are  rapidly  ascending  in  progress  and  run  a 
quickly  fatal  course.  It  is  sometimes  very  difficult  to 
say  whether  a  case  is  one  of  Landry's  paralysis  in  the 
strict  sense,  or  one  of  the  cases  that  depend  on  a  multi- 
ple neuritis.  The  points  to  be  especially  studied  in  such 
a  case  are  the  sensory  symptoms,  the  state  of  nutrition  of 
the  muscles,  and  the  electrical  reactions.  Another  point 
of  some  importance  is  the  fact  that  in  multiple  neuritis 
bulbar  symptoms  are  usually  slight  or  absent,  while  in 
acute  ascending  paralysis  they  are  almost  constant.  Ex- 
tensive poliomyelitis,  involving  the  lumbar,  cervical,  and 
bulbar  centres  may  simulate  acute  ascending  paralysis, 
but  the  early  appearance  of  muscular  atrophy  and  RD, 
and  the  absence  of  sensory  symptoms  sufficiently  indi- 
cate the  nature  of  the  condition  in  such  cases. 

Cases  of  acute  ascending  paralysis  differ  considerably 
in  the  rate  of  their  progress.  In  many  cases  they  end 
fatally  within  a  week.  Sometimes  they  run  their  course 
and  terminate  fatally  within  two  days.  In  other  in- 
stances the  disease  runs  a  course  of  two,  three,  or  four 
weeks.  Most  cases  that  have  been  reported  as  instances 
of  recovery  from  acute  ascending  paralysis  have  prob- 
ably been  cases  of  multiple  neuritis  or  myelitis. 

It  has  been  thought  that  some  of  these  cases  are  instances  of  mye- 
litis of  a  peculiar  type,  but  there  is  little  to  support  the  view. 


CHAPTER  VI. 

THE    DISTINCTION    OF    FUNCTIONAL    AND    ORGANIC 
DISEASE. 

The  distinction  of  functional  and  organic  disease  of 
the  nervous  system  constitutes  a  general  diagnostic  prob- 
lem of  the  highest  importance.  The  object  of  correct 
diagnosis  being  accurate  prognosis  and. rational  treat- 
ment, it  needs  no  argument  to  show  how  necessary  is 
the  clear  separation  of  processes  that  involve  actual  de- 
struction or  alteration  of  tissue,  and  limited  power  of 
repair,  from  those  which  consist  in  disorders  of  function 
and  nutrition  with  practically  unlimited  possibilities  of 
recovery. 

The  terms  "functional  disease"  and  ''organic  dis- 
ease" are  cpmmonly  employed  in  the  case  of  the  nervous 
system,  as  with  other  parts,  in  an  antithetical  sense. 
We  picture  to  ourselves,  on  the  one  hand,  a  class  of 
morbid  conditions  in  which  the  symptoms  depend  on 
demonstrable  structural  changes  in  nerve-elements,  or 
their  vascular  and  connective-tissue  belongings,  and,  on 
the  other,  a  category  of  cases  in  which  the  symptoms  are 
due  to  disorders  of  function  alone,  without  correlative 
changes  in  structure.  But  such  separation  of  categories 
is,  in  part  at  least,  erroneous.  A  functional  disease  is 
strictly  speaking  a  derangement  of  function  without  a 
pre-existing  alteration  in  nutrition.  The  cases  that 
actually  belong  in  this  class  are  probably  very  few,  and 

556 


FUNCTIONAL  AND   ORGANIC   DISEASE.         557 

are  separated  by  a  wide  gap  from  the  class  of  undoubted 
organic  disease.  In  this  gap  lies  a  large  class  of  cases 
in  which  alteration  in  the  nutrition  of  nerve-elements 
may  be  assumed  to  underlie  disordered  function.  In 
some  cases  these  nutritional  changes  are  slight,  in 
others  they  are  profound,  and  it  is  readily  to  be  con- 
ceived that  a  state  is  often  reached  in  which  the  nutri- 
tional alterations  reach  a  point  where  slight  alterations 
in  structure  make  their  appearance.  There  is  every 
conceivable  gradation,  it  should  seem,  between  the  disease 
that  is  purely  functional  and  the  marked  changes  of 
organic  disease,  and  experience  teaches  that  many  of  the 
functional  disorders  of  one  generation  are  classed  with 
organic  diseases  in  the  next,  under  the  influence  of  im- 
proved microscopical  technique.  The  antithetical  terms 
"'  organic  disease  "  and  ^'  functional  disease  "  may  desig- 
nate with  sufficient  accuracy  the  extreme  types  of  disease, 
but  do  not  cover  satisfactorily  the  transitional  territory 
between,  and  their  inadequacy  must  be  borne  in  mind 
when  they  are  employed  in  the  wide  and  rather  loose 
sense  which  convenience  and  custom  sanction. 

It  is  designed  in  this  chapter  to  touch  upon  the 
salient  features  of  the  various  forms  of  functional  (and 
nutritional)  disease  of  the  nervous  system  in  their  relation 
to  diagnosis,  special  stress  being  laid  on  the  distinction 
of  forms  which  simulate  organic  disease. 

The  great  type  of  functional  disease  of  the  nervous 
system  is  hysteria,  and  we  may  well  commence  with  a 
consideration  of  its  characteristics. 

Hysteria. — The  word  hysteria  is  employed  to  desig- 
nate a  morbid  state  of  the  nervous  system  which  is 
especially  common  in  the  female  sex  during  the  period 
of  adolescence  and  early  adult  life,  and  which  consists, 
broadly    speaking,   in    a    primary    derangement    of   the 


558        DISEASES   OF  THE  NERVOUS   SYSTEM. 

highest  cerebral  centres,  through  which  lower  centres, 
both  in  the  brain  and  in  the  cord,  may  become  more  or 
less  extensively  involved  in  a  secondary  manner.  The 
variety  of  these  secondary  derangements  of  lower  cen- 
tres give  to  hysterical  disorders  a  latitude  of  range  which 
constitutes  one  of  the  most  striking  features  of  a  remark- 
able malady.  In  the  category  of  the  symptoms  of 
hysteria  is  included  almost  every  symptom  known  to 
organic  disease.  Here  are  found  paralyses,  spasm  and 
contracture,  convulsive  seizures,  states  of  disordered 
consciousness,  as  stupor  and  coma,  mental  disorders,  dis- 
turbances in  gait  without  paralysis,  headache  and  pain 
of  almost  every  kind  and  distribution,  speech  disorders, 
and  the  ipaost  varied  disturbances  of  general  and  special 
sensibility. 

These  varied  forms  of  hysterical  manifestation  may, 
in  their  various  clinical  combinations,  present  a  close 
resemblance  to  certain  forms  of  organic  disease.  There 
are,  however,  certain  broad  characters  that  are  com- 
monly possessed  by  the  hysterical  conditions,  which 
often  serve  in  making  the  distinction  from  organic 
disease. 

Firsi^  there  is  the  circumstance  that  hysterical  dis- 
orders very  commonly  develop  after  emotional  disturb' 
ance,  as  after  fright,  grief,  or  anger.  Often,  also,  the 
onset  of  the  symptoms  follows  immediately  on  an  injury 
which  is  slight  in  degree  and  out  of  all  proportion  to 
the  extent  and  apparent  gravity  of  the  consecutive  symp- 
toms. A  careful  inquiry  in  such  cases  will  generally 
show  that  with  this  slight  trauma  was  associated  a 
considerable  degree  of  emotional  disturbance.  In  some 
cases  the  hysterical  symptoms  come  on  after  the  patient 
has  witnessed  similar  or  remotely  analogous  symptoms 
in  another   person — as,   for   example,    where  hysterical 

34 


FUNCTIONAL  AND   ORGANIC  DISEASE.         559 

tremor  develops  in  a  patient  who  has  lived  with  a  case 
of  chorea. 

Secondly^  there  is  the  fact  that  hysterical  symptoms 
often  increase  distinctly  on  attention.  During  examina- 
tion many  symptoms  may  become  aggravated.  When 
such  increase  under  attention  occurs  it  is  a  highly 
significant  sign  ;  but  it  is  frequently  absent,  and  hence 
its  absence  has  little  negative  significance. 

Thirdly^  the  symptoms  of  hysteria  are  frequently 
unsettled.  They  may  vary,  not  only  under  attention, 
but  without  apparent  cause.  Symptoms  of  one  kind 
may  disappear  suddenly  or  rapidly,  to  be  followed  by 
others  of  a  different  character, — in  fact,  of  a  character  so 
different  that  they  could  not  be  referred  to  the  same 
organic  process.  Thus  the  hemi-anaesthesia  which  is 
right-sided  one  day  is  left-sided  the  next  ;  or,  to  take  a 
less  uncommon  instance,  a  paralysis  which  is  complete, 
becomes  within  a  few  hours  partial  in  degree.  Again, 
anaesthesia  and  hyperalgesia  may  rapidly  alternate  with 
one  another.  This  mutability  in  the  character  of  the 
symptoms  is  highly  distinctive  of  hysteria. 

But  the  most  important  element  in  the  diagnosis 
between  hysteria  and  organic  disease  is  the  fact  that 
differences  actually  exist,  in  the  majority  of  instances, 
between  symptoms  that  are  hysterical  and  the  corre- 
sponding and  similar  symptoms  of  organic  origin. 

As  examples  of  these  differences,  we  may  take  different 
types  of  paralysis  :  the  monoplegic  type,  the  paraplegic 
type,  and  the  hemiplegic  type,  and  compare  the  func- 
tional (hysterical)  form  with  the  organic'    . 

An  hysterical  monoplegia  may  involve  either  arm  or 
leg — more  frequently  the  former, — and  may  be  of  sud- 
den or  gradual  onset.  The  paralysis  may  be  complete 
or  partial ;  it  is  rarely  complete  from  the  onset.     The 


560        DISEASES   OF  THE   NERVOUS   SYSTEM. 

paralysis  has  a  segmental  distribution, — i.e.,  the  distribu- 
tion characteristic  of  paralysis  of  cerebral  origin  ;  the 
muscles  of  the  hand  are  involved,  or  the  muscles  of  the 
hand  and  forearm,  or  of  the  hand,  forearm,  and  arm. 
This  segmental  character  of  the  paralysis  distinguishes 
it  (generally  speaking)  from  nerve-palsies,  where  the 
paralysis  corresponds  to  definite  nerve  distribution,  and 
from  spinal  paralysis,  in  which  functionally  related  groups 
of  muscles  are  involved. 

If  the  paralyzed  muscles  are  contractured,  this  con- 
tracture presents  a  characteristic  which  is  distinctive  of 
all  hysterical  contractures,  namely,  that  when  an  effort 
is  made  to  reduce  the  contracture,  the  resistance  ex- 
perienced is  not  uniform,  but  varies  from  instant  to 
instant  and  gives  the  impression  of  spasmodic  voluntary 
resistance. 

This  is  a  very  important  point  of  distinction  between 
hysterical  and  cerebral  (organic)  paralyses. 

In  an  hysterical  monoplegia  the  paralyzed  muscles  never 
undergo  any  considerable  degree  of  atrophy.  The  limb 
may,  indeed,  grow  flabby,  and  in  time  undergo  such 
slight  diminution  in  bulk  as  occurs  from  disuse  ;  but 
there  is  no  such  wasting  as  is  regularly  seen  in  the 
paralyses  of  spinal  and  neural  origin.  The  electrical 
reactions  are  at  first  normal,  and  may  be  normal  through- 
out, but  in  many  instances  the  slight  wasting  from  disease 
is  associated  with  slight  alterations  in  the  irritability  of 
the  muscles  {vide  page  173).  The  RD  is  never  observed 
even  in  its  partial  forms. 

Hysterical  monoplegias  may  be  unassociated  with  any 
alteration  in  the  sensibility  of  the  skin  overlying  the 
paralyzed  muscles  ;  but  often  there  are  sensory  changes. 
When  present,  these  sensory  changes  are  often  distinctive 
in  character. 


FUNCTIONAL  AND   ORGANIC   DISEASE.         56 1 

The  most  important  general  characteristic  of  the 
anaesthesias  and  analgesias  of  hysterical  monoplegias  is 
their  segmental  distribution.  Instead  of  corresponding 
to  the  distribution  of  one  or  more  nerve  trunks,  as  is  the 
case  with  the  anaesthesias  and  analgesias  of  peripheral 
and  spinal  origin,  they  correspond  in  general  to  the  seg- 
ments of  the  limb  affected — hand,  hand  and  forearm, 
or  hand,  forearm,  and  arm — if  it  be  the  upper  extremity. 
In  respect  to  this  segmental  distribution  the  hysterica] 
anaesthesias  resemble  the  anaesthesias  that  result  from 
organic  cerebral  disease.  There  is,  however,  one  impor- 
tant point  of  difference  which  is,  as  a  rule,  available.  In 
the  anaesthesia  that  accompanies  an  hysterical  monoplegia 
the  loss  of  sensibility  extends  to  a  certain  level  on  the 
limb,  and  then  ends  abruptly,  but  in  the  loss  of  sensibility 
that  accompanies  a  monoplegia  due  to  a  cerebral  lesion, 
the  sensory  loss  (which  is  commonly  slight  in  degree  and 
limited  in  extent)  fades  gradually  from  the  periphery 
towards  the  central  end  of  the  limb.  These  points  of 
distinction  will  serve  to  distinguish  even  the  cases  of 
hysterical  monoplegia  in  which  the  general  indications 
of  hysteria  are  equivocal. 

Under  the  designation  "  hysterical  paraplegia "  are 
included  several  conditions,  which,  though  closely  allied, 
should  be  clearly  distinguished.  The  first  class  of  cases 
comprises  those  in  which  there  is  a  purely  cerebral 
derangement  of  control  over  the  lower  extremities — a 
paralysis  of  volition,  without  even  secondary  functional 
derangement  of  the  spinal  cord.  The  central  functions 
of  the  cord  are  preserved  ;  the  reflexes,  superficial  and 
deep,  are  normal  ;  there  is  no  affection  of  the  sphincters, 
and  the  muscles  show  little  or  no  wasting.  But  the 
patient  cannot  move  her  legs,  or  can  move  them  only 
slightly  ;  only  rarely  is  the  loss   absolute.      When    the 


562         DISEASES   OF  THE  NERVOUS   SYSTEM. 

patient  makes  an  effort  to  overcome  resistance,  the  group 
of  muscles  chiefly  concerned  in  the  act  is  antagonized  in 
a  hesitating  or  jerky  manner  by  the  opposing  muscles, 
and  the  resulting  movement  is  irregular  and  jerky. 
Sometimes  when  an  attempt  is  made  to  obtain  the  knee- 
jerk,  a  contraction  of  the  extensors  of  the  knee  is  pre- 
vented by  a  semi-voluntary  contraction  of  the  antago- 
nistic flexors.  This  may  create  the  erroneous  impression 
that  no  knee-jerk  is  present. 

In  some  of  these  cases  of  hysterical  paraplegia  there 
is  some  loss  of  sensibility  of  the  legs,  but  it  is  usually 
slight  in  degree.  It  is  scarcely  conceivable  that  such  a 
case  should  be  confounded  with  an  organic  affection  of 
the  cord,  but  with  cases  of  the  second  class  of  "hysteri-, 
cal  paraplegias "  such  an  error  may  be  more  readily 
made. 

The  important  characteristic  of  the  cases  of  the 
second  class  is  that  they  present  distinct  evidence  of 
disordered  function  of  the  spinal  cord.  In  addition 
to  considerable  or  slight  loss  of  power  in  the  lower 
extremities,  there  is  an  increase  in  the  myotatic  irrita- 
bility of  the  leg  muscles.  The  knee-jerks  are  increased, 
and  may  be  obtained  by  striking  the  quadriceps  tendon 
above  the  patella.  In  rare  cases  there  may  be  obtained 
a  true  ankle  clonus,  but  more  often  there  is  merely  a 
semi-voluntary  jerky  spasm,  known  as  the  "spurious 
clonus."  There  may  be  retention  of  urine,  but  never 
incontinence,  either  of  urine  or  faeces.  There  is  often 
some  spinal  pain  and  tenderness  in  the  lumbar  region, 
but  never  a  cincture  pain.  The  legs  may  be  flabby,  but 
never  waste,  and  never  present  the  RD.  Sensibility  is 
only  slightly  or  not  at  all  affected.  Attention  to  these 
points  of  distinction  from  paraplegia  of  organic  origin 
will  prevent  an  error  of  diagnosis. 


FUNCTIONAL   AND   ORGANIC   DISEASE.  563 

The  last  variety  of  hysterical  paraplegia  to  be  men- 
tioned differs  little  in  its  symptoms  from  that  just 
described.  But  it  differs  in  its  history  in  this  important 
respect,  that  the  symptoms  of  disordered  function  of  the 
cord  are  merely  aggravated  by  the  development  of  the 
hysterical  state,  and  are  preceded  by  a  considerable 
period  in  which  the  patients  have  had  slight  symptoms 
of  spinal  cord  disturbance,  which  are  not  due  to  hysteria. 
These  symptoms  are  slight  weakness  in  the  legs,  fatigue 
on  slight  exertion,  spinal  pain,  and  flabby  muscles, 
occurring  usually  in  women  in  depressed  health  from 
any  cause  (  but  especially  prolonged  anaemia  and  debili- 
tating febrile  diseases).  When  hysterical  symptoms 
develop  in  such  women,  the  existent  spinal  symptoms 
("spinal  weakness")  determine  the  direction  of  de- 
velopment of  the  hysterical  symptoms,  and  hysterical 
paraplegia  results. 

Hysterical  hemiplegia  may  be  readily  distinguished 
from  hemiplegia  of  organic  origin  by  the  following  char- 
acters :  In  hysterical  hemiplegia  the  face  is  never 
involved  ;  in  organic  hemiplegia  the  face  rarely  escapes, 
unless  the  arm  and  leg  are  very  slightly  involved  or 
the  lesion  is  in  the  pons  or  medulla.  The  contractures 
of  hysterical  hemiplegia  have  the  characters  noted  in 
connection  with  hysterical  monoplegias  (p.  531).  The 
skin  reflexes  are  generally  normal,  never  lessened,  as  at 
the  onset  of  organic  hemiplegia.  The  knee-jerks  are 
usually  equal,  not  increased  on  the  paralyzed  side. 
There  is  never  an  ankle  clonus  on  the  paralyzed  side 
unless  there  is  great  contracture  of  the  posterior  tibial 
group,  but  a  '' spurious  clonus"  is  sometimes  obtained 
when  there  is  no  contracture. 

In  hysterical  hemiplegia  the  loss  of  power  is  never 
absolute,  as  it  so  often  is  in  the  organic  paralysis,  and 


564        DISEASES   OF   THE  NERVOUS   SYSTEM. 

the  leg  is  not  rarely  more  aifected  than  the  arm.  When 
progression  is  possible,  it  is  different  in  hysterical  and 
organic  hemiplegia.  In  the  former,  the  affected  leg  is 
brought  nearly  straight  forward  from  behind,  the  toes 
trailing  on  the  ground  ;  in  the  organic  paralysis  the 
palsied  leg  is  advanced  with  a  marked  lateral  movement, 
the  foot  being  thrown  out  in  such  a  way  as  to  describe 
the  arc  of  a  circle.  In  most  cases  of  hysterical  hemi- 
plegia there  is  anaesthesia  of  the  paralyzed  side.  It  may 
involve  the  whole  of  one  side,  including  the  face 
( hemianaesthesia ),  or  may  affect  chiefly  the  arm  or  the 
leg.  In  cases  of  hemianaesthesia  the  special  senses  are 
implicated  in  the  peculiar  manner  described  elsewhere 
(p.  127).  The  onset  of  hysterical  hemiplegia  is  often 
rapid,  but  is  never  sudden,  as  is  the  case  with  vascular 
lesions  that  cause  hemiplegia.  It  is,  moreover,  never 
accompanied  with  loss  of  consciousness. 

The  occasional  cases  of  bilateral  hysterical  hemiplegia, 
with  bilateral  or  one-sided  anaesthesia,  cannot  be  con- 
founded with  bilateral  organic  hemiplegia  if  the  facts 
relating  to  the  distinction  of  hysterical  hemiplegia  are 
borne  in  mind. 

The  most  common  form  of  hysterical  paralysis  is 
adductor  palsy  of  the  larynx,  with  resulting  aphonia.  It 
is  important  and  easy  to  distinguish  this  form  of  palsy 
from  organic  laryngeal  palsies.  Its  characters  are  highly 
distinctive  :  there  is  loss  of  voice,  but,  notwithstanding 
this,  the  cough  is  in  most  instances  perfect.  In  all 
other  laryngeal  palsies  loss  of  phonation  is  associated 
with  loss  of  cough.  In  local  affections  of  the  larynx, 
such  as  laryngitis,  there  is  always  an  effort  to  phonate, 
with  resulting  hoarseness.  Inspection  of  the  larynx  in  a 
case  of  hysterical  aphonia  shows  that  the  cords  move 
normally    during    respiration,   but    that    they    are    not 


FUNCTIONAL  AND    ORGANIC   DISEASE.  565 

approximated  when  the  patient  attempts  to  speak.  Very 
rarely  abductor  paralysis  of  the  vocal  cords  occurs  as  an 
hysterical  affection,  with  laryngeal  symptoms  like  those 
of  the  organic  form  of  the  same  paralysis.  The  diag- 
nosis here  depends  on  evidence  of  an  associated  hys- 
terical affection. 

A  form  of  hysterical  disturbance  known  as  astasia- 
abasia  is  liable  to  be  confounded  with  inco-ordination 
due  to  organic  disease.  This  condition,  when  typically 
developed,  consists  of  an  inability  to  stand  without 
swaying  violently  from  side  to  side,  and  of  an  inability 
to  walk  without  a  side-to-side  staggering  motion,  due  to 
the  alternate  and  violent  contraction  of  antagonistic 
muscles.  There  is  no  ataxia,  strictly  speaking.  If  the 
patient  be  steadied  in  the  erect  position  the  toes  are 
readily  guided  into  contact  with  neighboring  objects. 
The  upper  extremities  are  entirely  free  from  irregularity 
of  movement,  and  when  the  patient  lies,  control  over  the 
lower  extremities  is  perfect.  Sometimes  the  defect  is 
hemiplegic  in  distribution.  The  knee-jerks  are  often 
increased,  and  the  condition  is  often  associated  with 
unmistakable  signs  of  hysteria.  These  characters  serve 
to  separate  the  condition  from  the  inco-ordination  of 
spinal  and  cerebellar  disease.  In  its  fully  developed 
form  and  as  the  dominant  symptom  of  hysteria,  this 
condition  is  rare.  A  slighter  grade  of  the  disturbance 
with  other  hysterical  manifestations  is  common.  It 
appears  not  to  depend  on  cutaneous  anaesthesia. 

Hysterical  internal  strabismus  may  be  confounded  with 
organic  paralysis  of  ocular  muscles,  unless  it  is  remem- 
bered that  it  is  due  to  spasm,  and  that  the  absence  of 
paralysis  may  be  demonstrated  by  testing  the  muscles  of 
each  eye  with  the  other  closed.  Hysterical  ptosis,  when 
single,  is  easily  detected  by  asking  the  patient  to  look  up. 


566        DISEASES   OF   THE   NERVOUS   SYSTEM. 

when  the  orbicularis  spasm  on  which  it  depends  becomes 
exaggerated  in  order  to  prevent  the  lid  from  moving  up. 
When  double,  the  head  is  thrown  back  when  the  patient 
is  requested  to  look  up. 

The  convulsive  paroxysms  of  hysteria  are  distinguished 
by  their  associations  from  the  convulsions  of  acute  organic 
disease  and  by  their  general  distribution,  irregular  charac- 
ter, and  tendency  to  extensor  spasm,  from  the  locally  com- 
mencing seizures  that  characterize  chronic  focal  lesions 
of  the  brain. 

There  are  other  hysterical  conditions  besides  those 
mentioned  here  that  have  been  confounded  with  organic 
disease  of  the  nervous  system,  but  it  is  believed  that  the 
points  of  distinction  given  here  and  in  the  chapter  on 
symptomatology  will  suffice  in  the  great  majority  of  in- 
stances for  the  separation  of  the  hysterical  from  the 
organic  conditions.  But  certain  general  facts  regarding 
conditions  that  appear  to  be  of  hysterical  origin  remain 
to  be  emphasized.  The  first  step  in  the  diagnosis  of  any 
condition  in  which  there  is  a  suspicion  or  distinct  evi- 
dence of  hysteria  is  to  look  most  carefully  for  symptoms 
that  indicate  the  presence  of  organic  disease,  and  not 
until  such  disease  has  been  excluded  is  it  safe  to  assume 
that  the  hysterical  manifestations  present  constitute  the 
primary  disease.  Many  women  who  are  the  subjects  of 
organic  disease  of  the  nervous  system  (as  multiple  sclero- 
sis and  certain  other  organic  brain  diseases)  suffer  also 
from  hysteria,  the  occurrence  of  which  is  determined  by 
the  presence  of  the  organic  disease.  It  is  therefore  evident 
that  until  the  possibility  of  a  primary  organic  condition 
has  been  eliminated,  even  the  most  pronounced  signs  of 
hysteria  in  a  woman  of  the  age  at  which  hysteria  prevails 
should  not  be  allowed  weight  as  to  the  nature  of  the 
primary  disease.     Close  attention  to  this  rule  will  prevent 


FUNCTIONAL   AND   ORGANIC   DISEASE.  567 

many  errors  in  diagnosis.  When,  as  occasionally  occurs, 
the  symptoms  appear  distinctive  of  neither  hysteria  nor 
organic  disease,  and  are  to  all  appearances  quite  inde- 
cisive, a  diagnosis,  if  possible,  must  be  based  on  a  knowl- 
edge of  the  differences  (which  almost  always  exist)  in  the 
minute  characters  and  associations  of  the  symptoms  com- 
mon to  the  two  different  states. 

The  Traumatic  Neurosis  or  Psycho-Neurosis.' 
— It  is  generally  acknowledged  that  many  forms  of  injury 
that  are  accompanied,  at  the  time  of  their  infliction,  with 
a  considerable  degree  of  mental  shock  (railroad  injuries 
especially),  are  followed,  after  a  variable  period,  by  ner- 
vous symptoms  varying  widely  in  character  in  different 
cases,  but  agreeing  in  this,  that  they  indicate  a  more  or 
less  general  disturbance  of  cerebral  function.  The  symp- 
toms in  some  of  these  cases  suggest  cerebral  disturbance 
of  the  most  purely  functional  type.  In  fact,  these  cases 
possess  the  characters  that  have  been  described  as  dis- 
tinctive of  hysteria,  and  such  have  been  very  appropri- 
ately designated  "  traumatic  hysteria."  Often  the  subjects 
are  males  who  have  some  neurotic  predispositions.  In 
some  cases  the  symptoms  are  such  as  indicate  purely 
general  cerebral  disturbance ;  in  others  local  symptoms, 
as  monoplegic  or  local  sensory  disturbance,  are  especially 
obtrusive.  But  even  in  these  cases  the  cerebral  and 
functional  nature  of  the  symptoms  is  plainly  shown  by 

^  Actual  simulation  of  symptoms  of  a  traumatic  neurosis  is  very 
rare,  but  voluntary  exaggeration  of  symptoms  actually  present  is  rela- 
tively common.  It  is,  however,  not  often  encountered  in  hysteria. 
In  neurasthenics  the  making  the  most  of  symptoms  is  not  only  an  im- 
portant part  of  the  disease,  but  is  inseparable  from  it.  It  is  often 
difficult  to  say  whether  a  patient  exaggerates  in  spite  of  himself  or 
intentionally.  Some  help  may  be  gained  from  information  obtained 
from  outside  sources. 


568         DISEASES   OF  THE  NERVOUS   SYSTEM. 

the  nature  of  the  local  symptoms  and  by  their  associa- 
tion with  more  general  hysterical  manifestations.  The 
criteria  of  distinction  from  organic  disease  are,  of 
course,  the  same  in  these  cases  as  those  that  have  been 
described  in  the  preceding  section  i^vide  Hysteria). 

But  there  remains  a  large  and  important  class  of  cases 
in  which  the  symptoms  following  injury  and  mental  fright 
(shock)  are  such  as  to  suggest,  by  their  character  and 
permanency,  a  graver  condition  than  can  properly  be  in- 
cluded even  under  the  broad  term  hysteria.  There  is 
good  reason  to  believe  that  the  symptoms  in  these  cases 
cannot  be  referred  to  a  mere  disturbance  of  function, 
but  depend  on  nutritional  alterations  in  nervous  elements, 
which  vary  in  degree  in  different  cases,  and  which  may 
even  consist,  in  some  instances,  in  fine  structural  changes 
at  present  beyond  the  cognizance  of  histology.  The 
cases  belonging  to  this  class  present  important  differences 
in  the  severity  of  their  symptoms,  and  fade  imperceptibly, 
on  the  one  hand,  into  the  severer  forms  of  traumatic 
hysteria,  and,  on  the  other,  into  the  milder  forms  of 
diffuse  and  focal  organic  disease  of  the  brain. 

The  term  "  traumatic  neurosis  "  has  been  and  is  still 
used  to  designate  this  class  of  cases,  but  its  use  is  open  to 
the  objection  that  it  implies  a  distinct  and  specific  form 
of  cerebral  disturbance,  whereas  it  must  be  owned  that 
the  cases  included  in  the  term  may  and  probably  do  differ 
considerably  in  their  pathology.  But  the  name  is  con- 
venient, and  the  objection  to  its  use  is  much  reduced  if 
it  be  borne  in  mind  that  it  probably  does  not  designate 
a  pathological  entity.  Those  who  wish  to  emphasize  the 
characteristic  and  obtrusive  psychical  element,  use  the 
term  "  traumatic  psycho-neurosis." 


FUNCTIONAL  AND   ORGANIC  DISEASE.  569 

The  traumatic  neurosis*  regularly  presents  symptoms 
which  cannot  be  purely  functional  in  character,  and  it  ap- 
pears an  unwarrantable  extension  of  the  term  hysteria  to 
make  it  include  forms  of  disease  that  are  so  stable  in  symp- 
tomatology that  they  must  depend  on  decided  nutritional 
alterations  in  nervous  tissues.  The  "traumatic  neurosis" 
is  as  much  entitled  to  a  separation  from  hysteria  as  are 
the  numerous  cases  of  chorea  that  follow  fright.  But  it 
must  be  owned,  even  by  the  most  zealous  advocates  of 
the  traumatic  neurosis,  that  there  are  cases  on  the  border- 
land between  hysteria  and  the  traumatic  neurosis,  which 
it  is  difficult  to  classify,  and  about  whose  classification 
there  is  room  for  a  just  difference  of  opinion.  There  are 
also  cases  in  which  hysterical  symptoms  are  mixed  with 
symptoms  of  the  traumatic  neurosis,  which  cause  great 
difficulties  in  diagnosis.  It  must  be  owned,  furthermore, 
that  the  entire  subject  of  traumatic  hysteria  and  the  trau- 
matic neurosis  is  beset  with  difficulties  and  is  likely  for 
a  long  time  to  come  to  afford  opportunity  for  the  expres- 
sion of  widely  different  views. 

x\fter  a  brief  description  of  the  main  clinical  features 
of  the  traumatic  neurosis  will  be  presented  the  main 
points  of  distinction  from  hysteria. 

^  Some  writers  contend  that  the  traumatic  neurosis  is  merely  a  com- 
bination of  hysteria  and  neurasthenia.  They  hold  that  trauma  acts  in 
these  cases  by  causing  a  kind  of  mental  over-strain,  the  short  duration 
of  the  influence  being  compensated  by  its  intensity.  There  can  be 
little  doubt  that  trauma  may  lead  to  the  development  of  combined 
hysterical  and  neurasthenic  symptoms,  but  this,  we  take  it,  does  not 
constitute  the  traumatic  neurosis.  The  severity  of  the  symptoms  in 
most  cases  of  the  traumatic  neurosis,  and  their  rapid  onset  in  many 
instances,  would  serve,  it  should  seem,  to  completely  separate  at  least 
these  cases  from  any  that  may  reasonably  be  termed  neurasthenia. 


570        DISEASES   OF  THE   NERVOUS   SYSTEM. 

The  symptoms  of  the  traumatic  neurosis  come  on  within 
a  short  time  of  the  injury  and  fright,  or,  as  happens  with 
equal  frequency,  they  do  not  appear  for  weeks  or  months 
afterwards. 

In  a  considerable  proportion  of  cases  the  patient  be- 
comes unconscious  for  a  short  period  (few  minutes)  after 
the  injury,  or  passes  temporarily  into  a  state  of  mental 
confusion.  Much  more  rarely  the  period  of  shock  lasts 
many  hours  or  even  days.  Sometimes  acute  insanity 
(hallucinatory  type)  follows  immediately  on  the  injury. 
In  most  cases  there  are  no  immediate  symptoms.  The 
patient  seems  perfectly  well  for  several  days — is  able  to 
work  as  usual,  etc.  Then  symptoms,  at  first  slight  and 
perhaps  overlooked,  make  their  appearance,  and  with  the 
lapse  of  time  (weeks  or  months)  become  gradually  more 
obtrusive.  Sometimes  the  original  surgical  injury  occu- 
pies the  sole  attention  of  the  patient  and  his  physician 
for  weeks  or  months,  the  symptoms  of  the  neurosis 
meanwhile  developing  insidiously. 

The  first  distinct  symptoms  are  usually  purely  subjec- 
tive in  character,  and  include  the  following : 

Pain,  especially  at  or  near  the  seat  of  injury,  and  when 
there  is  no  local  injury,  but  only  general  concussion,  espe- 
cially in  the  lower  dorsal,  lumbar,  and  sacral  regions. 
The  pain  is  increased  by  movement  in  the  part  affected, 
and  leads  to  some  limitation  of  motion. 

In  addition  to  pain,  which  is  almost  always  observed, 
there  are  usually  restlessness,  general  irritability,  and  very 
often  an  expression  of  anxiety.  The  mental  changes  grow 
rapidly  or  slowly  more  marked,  until  they  develop  into  a 
state  of  hypochondriacal  depression,  associated  commonly 
with  considerable  irritability.  Insomnia  is  a  frequent 
and  early  symptom.  It  is  rarely  absolute,  but  the  patient 
has  an  unquiet  sleep,  broken  by  frequent  cries  due  to  bad 
dreams.     General  tremor,  attacks  of  syncope^  and  occa- 


FUNCTIONAL   AND    ORGANIC   DISEASE.  571 

sional  convulsions  may  be  among  the  earlier  manifesta- 
tions of  the  disease.  The  intellectual  faculties  remain 
unaltered  or  only  slightly  changed.  Some  form  of  motor 
defect  is  of  almost  constant  occurrence.  The  loss  of 
power  is  usually  partial  and  often  very  slight.  The  distri- 
bution of  the  palsy  is  determined  partly  by  the  seat  of  the 
injury,  partly  by  other  circumstances.  All  four  extremi- 
ties may  be  slightly  paretic,  or  there  may  be  more  marked 
paralysis  of  hemi-,para-  or  monoplegic distribution.  These 
paretic  conditions  have  many  of  the  characters  of  the 
paralyses  of  hysteria  which  have  been  already  mentioned 
— there  is  little  or  no  atrophy,  and  the  electrical  reac- 
tions are  normal  or  show  only  slight  quantitative  changes. 
When  the  paralyses  are  monoplegic  they  show  a  distinct 
tendency  to  segmental  distribution,  never  the  distribution 
M^hich  corresponds  to  peripheral  nerves  or  spinal  segments. 
Occasionally  a  considerable  degree  of  atrophy  is  observed 
in  the  paralyzed  muscles,  with  distinct  histological  changes 
in  the  muscle-fibres. 

Sensory  symptoms  are  common  and  highly  character- 
istic. Very  often  there  is  partial  or  complete  hemianaes- 
thesia,  like  that  observed  in  hysteria,  with  alterations  in 
the  special  senses  on  the  same  side,  especially  concentric 
limitation  of  the  field  of  vision,  for  colors  and  for  white. 

A  variety  of  disturbances  of  speech  are  observed,  but 
there  is  never  aphasia.  Most  often  there  is  simple  slow- 
ing of  speech  ;  not  rarely  the  patient  brings  out  his  words 
in  an  irregular  and  uncertain  manner,  apparently  owing 
to  mental  excitement.  The  knee-jerks  are  very  often  in- 
creased, never  lost.  Occasionally  a  true  ankle  clonus  is 
obtained.  The  pupillary  reflex  is  usually  normal,  but  is 
sometimes  lost.  The  functions  of  the  bladder  and  rec- 
tum are  not  commonly  involved,  but  there  is  sometimes 
retention  of  urine,  as  in  hysteria.     Loss  of  sexual  desire 


572         DISEASES   OF  THE   NERVOUS   SYSTEM. 

IS  very  common.  (Edema  and  cyanosis  of  the  paralyzed 
extremities  are  not  rarely  observed. 

One  of  the  most  important  of  the  objective  symptoms 
of  the  traumatic  neurosis  is  tachycardia.  In  most  patients 
the  heart's  action  is  habitually  more  rapid  than  normal 
(90-130),  and  on  excitement  may  reach  130-140-150  or 
160  beats  per  minute.  Sometimes  this  condition  leads  to 
actual  cardiac  hypertrophy  and  dilatation. 

As  a  rule,  the  patients  who  suffer  from  the  condition 
described  grow  progressively  worse,  by  the  addition  of 
one  symptom  to  another,  and  by  the  gradual  or  rapid 
advance  of  those  that  first  appear. 

After  a  variable  period  the  condition  either  slowly  im- 
proves or  settles  into  a  chronic  state,  with  slight  alterations 
for  the  better  or  worse.  The  prognosis  as  regards  life  is 
good  ;  as  regards  recovery  it  is  bad.  Among  the  most  per- 
sistent and  unchanging  symptoms  are  the  mental  alterations. 

The  injury  that  gives  rise  to  the  traumatic  neurosis  varies 
much.  There  may  be  a  slight  or  considerable  local  inju- 
ry, or  there  may  be  merely  a  general  concussion.  The 
gravity  of  the  disease  appears  to  bear  no  fixed  relation  to 
the  severity  of  the  injury.  It  is,  however,  greatly  influ- 
enced by  the  mental  shock  that  constantly  accompanies 
these  cases.  Indeed,  it  is  to  this  regular  accompaniment  of 
the  trauma  that  the  peculiar  character  of  the  disease  ap- 
pears to  be  due.  That  severe  mental  shock  is  the  essen- 
tial element  in  the  causation  of  the  neurosis  is  shown  by 
the  occasional  occurrence  of  cases  of  typical  character  in 
which  the  mental  shock  has  been  profound  but  physical 
injury  could  not  be  detected. 

Among  the  criteria  that  serve  for  the  distinction  of 
the  traumatic  neurosis  from  traumatic  hysteria  are  the 
following  : 

I.    The  Greater  Fixity  of  the  Symptoms  which  the  two 


FUNCTIONAL  AND   ORGANIC   DISEASE.  573 

conditions  have  in  common.  This  is  especially  notice- 
able in  the  sensory  symptoms.  The  hemianaesthesia  of 
the  traumatic  neurosis  is  subject  to  relatively  slight  vari- 
ations in  distribution  and  intensity  ;  there  is  never  a 
transfer  or  a  rapid  change  in  the  degree  of  anaesthesia. 
This  greater  fixity  is  also  very  striking  in  the  case  of  the 
mental  symptoms.  There  are,  indeed,  changes,  but  these 
are  not  considerable  within  short  periods  of  time,  and  the 
general  nature  of  the  mental  disturbance  remains  the  same, 
whilst  in  hysteria  it  may  vary  much.  A  similar  but  less 
striking  difference  in  the  permanence  of  symptoms  is 
noted  in  the  motor  and  vaso-motor  disturbances. 

II.  The  traumatic  neurosis  generally  occurs  in  per- 
sons who  have  no  recognizable  neurotic  predisposition, 
and  who  have  been  otherwise  healthy.  It  is  very  rare, 
on  the  contrary,  to  find  cases  of  hysteria  of  equal  gravity, 
in  which  a  neurotic  predisposition  is  not  traceable  or 
even  obtrusive.  This  is  an  exceedingly  important 
etiological  point  of  distinction. 

III.  Differences  in  the  Symptoms  Themselves. — While 
there  is  a  strong  general  resemblance  between  many  of 
the  symptoms  of  the  two  conditions,  there  are  important 
differences  in  the  grouping,  detail,  frequency  of  occur- 
rence and  character  of  certain  symptoms.  Thus  in  the 
traumatic  neurosis  the  mental  change  is  a  state  of 
hypochondriacal  depression,  a  dominant  and  charac- 
teristic condition.  In  hysteria  a  continuous  change 
of  this  nature  is  very  rare.  In  the  traumatic  neurosis, 
insomnia,  in  some  degree,  is  an  important  symptom, 
and  one  of  whose  existence  there  are  objective  proofs. 
If  present  in  traumatic  hysteria,  it  is  rarely  a  prominent 
symptom.  Distinct  muscular  atrophy,  histological  altera- 
tions in  the  muscle-fibres,  and  oedema  of  the  paralyzed 
extremities   are   more  often   observed  in   the   traumatic 


574         DISEASES   OF   THE   NERVOUS   SYSTEM. 

neurosis  than  in  traumatic  hysteria.  True  ankle 
clonus  is  not  uncommon  in  the  traumatic  neurosis  ; 
in  hysteria  it  is  rare.  An  important  and  common 
objective  condition  in  the  traumatic  neurosis  is  tachy- 
cardia. It  is  highly  characteristic  of  the  condition,  and 
is  not  a  co7itinuous  symptom  in  cases  of  pure  hysteria. 
Generally  speaking  the  symptoms  of  the  traumatic  neu- 
rosis are  symptoms  of  a  graver  character  than  those  of 
hysteria,  and  suggest  more  distinct  nutritional  changes 
in  the  nerve  elements.  Indeed  some  cases  of  the  trau- 
matic neurosis  show  conditions  that  can  be  referred  only 
to  anatomical  alterations  within  the  nervous  system 
(optic-neuritis,  optic  atrophy).  The  recognition  of 
gross  organic  lesions,  which  may  be  combined  with  the 
symptoms  of  the  traumatic  neurosis,  is  of  course  a  sim- 
ple matter.  But  it  is  no  easy  task,  indeed  it  is  often 
impossible,  to  state  whether  a  given  symptom  or  combi- 
nation of  symptoms  is  due  to  advanced  nutritional 
changes  or  to  slight  organic  changes.  It  is  important, 
however,  to  try  to  form  some  conception  in  each  case 
of  traumatic  neurosis  of  the  degree  of  the  nutritional 
changes  in  the  nervous  system.  The  great  point  to 
remember  is  that  we  have  to  deal  with  a  nutritional  dis- 
ease of  the  nervous  system,  which  in  its  graver  forms 
imperceptibly  shades  into  slight  organic  conditions  (optic 
neuritis,  optic  atrophy,  central  degenerative  changes,  as 
shown  by  loss  of  pupillary  reaction,  etc.),  which  for  pur- 
poses of  prognosis  it  is  extremely  important  to  detect. 
The  detection  of  such  conditions  can  be  accomplished 
only  by  making  a  systematic  search  for  the  slightest  un- 
equivocal sign  of  organic  disease.  It  is  unnecessary  to 
repeat  here  what  these  signs  are  (see  Paralysis,  Atrophy, 
Electrical  Reactions,  Ophthalmoscopic  Changes,  Convul- 
sions, Abnormal  Reflex  Action,  etc.). 

35 


FUNCTIONAL  AND   ORGANIC  DISEASE.  S7 D 

Neurasthenia '  is  a  nutritional  disease  of  the  brain 
due  to  disturbance  of  the  general  nutrition  of  the  body, 
resulting  especially  from  defective  assimilation  of  food. 
One  of  the  most  important  immediate  elements  in  the 
production  of  the  nervous  symptoms  is  a  vaso-motor 
instability  which  leads  to  continual  alterations  in  the 
blood-supply  of  the  brain.  Associated  with  this  condi- 
tion of  vaso-motor  instability  is  probably  an  alteration 
in  the  quality  of  the  cerebral  blood-supply,  but  of  this 
there  is  no  actual  knowledge. 

The  indirect  causes  of  the  disease  are  numerous,  but 
the  most  important  are  anxiety,  grief,  fright,  prolonged 
emotional  excitement,  and  sexual  excesses  and  mastur- 
bation. Not  rarely  neurasthenia  is  associated  with  hys- 
teria and  with  the  traumatic  neurosis. 

The  chief  symptoms  and  signs  of  neurasthenia  are  gen- 
eral debility,  defective  memory,  slight  diminution  in  will 
power,  abnormal  irritability,  mental  depression,  incapacity 
for  prolonged  mental  or  physical  exertion,  insomnia  or  ab- 
normal somnolence,  headache  (often  occipital),''  peculiar 
cephalic  sensations  (p.  140),  asthenopia,  palpitation, 
tachycardia,  fibrillary  contractions,  blepharospasm,  vari- 
ous dyspeptic  troubles,  night  sweats,  and  concentrated 
urine.^     While  many  of  these  symptoms. are  of  cerebral 

^  No  form  of  nervous  disease  is  of  such  common  occurrence  as  some 
degree  of  neurasthenia. 

^  The  headache  of  neurasthenia  is  never  severe,  and  is  exceedingly 
apt  to  be  temporarily  diminished  after  the  ingestion  of  food. 

^  There  are  few  cases  of  neurasthenia  which  do  not  show  in  the 
urine  or  fasces  some  indication  of  defective  metabolism.  The  condi- 
tions found  vary  considerably.  The  faeces  often  contain  excessive 
amounts  of  urobilin  or  some  related  substance.  The  urine  is  usually 
concentrated  and  of  small  volume  (600-1000  c.c.  in  24  hours).  Fre- 
quently there  is  an  excessive  excretion  of  phosphoric  acid  (PgOj),  and 
an  alteration  in  the  quantitative  relation  of  urea  and  uric  acid.     In 


5/6         DISEASES   OF   THE   NERVOUS   SYSTEM. 

origin,  many  others  are  due  to  visceral  disturbances,  but 
the  latter  may  be  entirely  absent.  Not  rarely  there  is 
associated  with  neurasthenic  symptoms  that  form  of 
mental  depression  which  is  due  to  false  ideas  of  bodily 
ailments  such  as  might  conceivably  exist,  viz.,  hypo- 
chondriasis. 

The  distinction  of  neurasthenia  from  other  forms  of 
functional  disease  gives  rise  to  no  difficulties,  but  it  is 
important  to  remember  how  often  it  occurs  with  such 
diseases.  Only  occasionally  is  there  difficulty  in  dis- 
tinguishing between  neurasthenia  and  organic  disease. 
The  cases  that  resemble  general  paralysis  of  the  insane 
are  elsewhere  considered  {j)ide  p.  400).  Fibrillary  contrac- 
tions may  be  very  persistent,  and  may  be  localized  for 
days  to  special  groups  of  muscles.  There  is  no  danger 
in  confounding  such  cases  with  progressive  muscular 
atrophy  if  the  associations  of  neurasthenia  are  borne 
in  mind.  Careful  inquiry  will  usually  show  that  the 
fibrillary  contractions  have  at  some  previous  time  been 
general  in  distribution.  Persistent  headache  may  be 
associated  with  local  spasm,  such  as  might  suggest  a  focal 
brain  lesion,  but  any  error  may  be  avoided  by  remem- 
bering that  the  local  spasm  of  neurasthenia  does  not 
recur  for  more  than  a  few  days  in  the  same  place,  and 
that  the  associations  of  neurasthenia  and  those  of  a 
focal  lesion  are  quite  different. 

Epilepsy. — Epilepsy  is  a  chronic  functional  (nutri- 
tional) disease  of  the  central  nervous  system  (brain), 
characterized  by  the  recurrence  at  irregular  intervals  of 

health  the  relation  of  the  uric  acid  to  the  urea  excreted  varies  between 
I  to  45  and  I  to  60  in  adults.  In  neurasthenia  (as  well  as  some  other 
conditions)  the  relation  is  often  i  to  40,  I  to  35,  or  I  to  30.  Indican  is 
often  present  in  pathological  quantities,  especially  in  cases  of  sexual 
neurasthenia.     Oxalate  of  lime  is  often  present  in  excess  in  the  urine. 


FUNCTIONAL  AND   ORGANIC   DISEASE.  577 

convulsive  seizures  of  a  certain  type,  or  by  the  sudden 
loss  or  impairment  of  consciousness,  or  by  a  combination 
of  these  conditions. 

For  clinical  purposes  it  is  convenient  to  classify  the 
different  forms  of  epilepsy  under  the  following  heads  : 

1.  Common  spasmodic  epilepsy  ("grand  mal,"  *' major 
seizures"). 

2.  Attacks  consisting  of  brief  loss  of  consciousness, 
with  or  without  slight  muscular  spasm,  or  (rarely)  of 
slight  muscular  spasm,  or  a  sudden  sensation  without 
actual  loss  of  consciousness  ('^  petit  mal,"  "minor  seiz- 
ures," improperly  called  "  epileptic  vertigo  "). 

3.  Attacks  consisting  qf  apparently  volitional  and  co- 
ordinated motor  or  mental  actions  during  a  state  of 
modified  consciousness.  The  mental  state  during  these 
attacks  differs  both  from  normal  consciousness  and  from 
the  unconsciousness  that  usually  occurs  in  epileptic 
attacks  ("psychical  epilepsy,"  "  psychical  epileptic  equiv- 
alent " — so-called  because  the  paroxysms  may  take  the 
place  of  typical  minor  seizures). 

These  different  forms  of  epilepsy  may  be  variously- 
combined  in  the  same  individual.  The  most  frequent 
combination  is  that  of  grand  mal  and  petit  mal. 

The  diagnosis  of  "  grand  mal,"  from  organic  disease  of 
the  brain  is  always  a  most  important  problem,  and  some- 
times an  exceedingly  difficult  one.  A  diagnosis  has  to 
be  made  from  cases  of  acute  cerebral  disease  (vascular 
lesions)  and  from  cases  of  chronic  cerebral  disease.  In 
epilepsy  the  convulsions  are  general,  tonic  spasm  is 
succeeded  by  clonic  spasm,  the  duration  of  the  attack  is 
short  (less  than  five  minutes),  the  attack  is  succeeded  by 
a  period  of  sleep  in  which  the  patient  may  be  partially 
aroused,  there  is  no  local  paralysis  (except  in  rare  cases 
of   unilateral    spasm  where  the  weakness  is  transient), 


578         DISEASES   OF   THE   NERVOUS   SYSTEM, 

there  is  often  a  history  of  repeated  attacks  of  a  similar 
character,  and  there  is  often  an  aura.  In  vascular 
lesions  of  the  brain,  on  the  contrary,  there  may  be  no 
convulsions,  and,  if  present,  they  are  chiefly  unilateral 
and  clonic  ;  loss  of  consciousness  is  usually  prolonged, 
there  is  hemiplegic  weakness  with  changes  in  reflex 
action  on  the  same  side,  and  if  the  attack  is  not  a  first 
one  the  number  of  preceding  attacks  is  small  (one  or 
two). 

In  the  diagnosis  of  epilepsy  and  chronic  brain  disease 
a  distinction  must  be  made  between  active  brain  disease 
and  old  retrogressive  lesions.  The  convulsions  of 
chronic  active  brain  disease  (tumor,  abscess,  chronic 
meningitis)  usually  have  a  local  commencement,  and 
are  often  partial  in  their  extension  {^nde  p.  82).  This 
is  a  most  important  point  of  distinction  from  idiopathic 
epilepsy  ;  but  it  must  be  remembered  that  it  is  not  an 
absolute  distinction,  for  the  convulsions  of  epilepsy 
sometimes  have  a  local  commencement,  and  the  convul- 
sions of  organic  brain  disease  may  have  a  general  and 
not  a  local  commencement.  Other  features  than  the 
convulsions  themselves  have  therefore  to  be  considered. 
It  is  essential  to  make  a  careful  inquiry  for  and  to  ex- 
clude all  evidences  of  organic  disease,  especially  severe 
and  persistent  headache,  persistent  hemiplegic  or  mono- 
plegic  weakness,  vomiting  without  gastric  cause,  optic 
neuritis,  and  paralysis  of  cranial  nerves. 

Certain  forms  of  retrogressive,  non-active  brain  disease, 
as  atrophic  tumors  (tubercular),  old  cases  of  so-called 
polioencephalitis  and  meningeal  hemorrhage  in  infancy, 
and  old  patches  of  softening,  may  give  rise  to  convulsive 
seizures  closely  resembling  attacks  of  grand  mal.  Often 
these  forms  of  disease  cause  permanent  hemiplegia,  and 


FUNCTIONAL  AND   ORGANIC   DISEASE.         579 

when  this  is  the  case  the  diagnosis  is  simple.  But  many 
of  the  cases  of  hemiplegia  of  infancy  recover  largely 
from  the  paralysis.  In  any  case,  therefore,  in  which 
convulsions  date  from  infancy,  and  especially  if  they  are 
unilateral,  careful  search  must  be  made  for  signs  of  an 
old  hemiplegia.  The  most  important  of  these  signs  are 
slight  hemiplegic  weakness,  hemiplegic  rigidity,  increased 
myotatic  irritability,  and  slight  retardation  of  growth  on 
the  weaker  side.  The  diagnosis,  in  many  instances,  de- 
pends on  these  objective  features  of  the  case,  as  the 
original  hemiplegia,  if  slight,  is  often  overlooked.  It  is 
important  to  note  that  the  first  recurrence  of  convulsions 
may  occur  a  long  time  (years)  after  the  convulsions  that 
attended  the  onset. 

In  seeking  to  discover  the  cause  of  the  paroxysms  in 
any  case  of  grand  mal,  it  is  important  to  study  the  pos- 
sible influence  of  injury  to  the  head.  A  not  inconsider- 
able number  of  cases  of  grand  mal  follow  closely,  in 
their  development,  upon  blows  or  falls  on  the  head. 
Many  of  these  cases  are  indistinguishable  by  their  symp- 
toms from  the  so-called  idiopathic  cases  of  epilepsy. 
Their  recognition  is  especially  important,  because  in  some 
instances  it  is  possible  to  relieve  them  by  operation.  In 
many  cases  local  changes  are  found  in  the  meninges.  It 
is  important,  also,  to  recognize  the  influence  which  dis- 
ordered nutrition  exerts  in  some  cases  of  apparently 
idiopathic  epilepsy  in  determining  the  occurrence  of 
paroxysms.  ^ 

^  The  most  important  evidence  of  such  nutritional  disorder  is  ob- 
tained by  a  study  of  the  urine.  In  some  cases  of  idiopathic  epilepsy 
(perhaps  a  considerable  proportion)  there  are  distinct  evidences  of 
abnormal  putrefactive  processes  in  the  small  intestine.  The  occur- 
rence of  such  processes  is  shown,  in  a  general  way,  by  a  disturbance 


58o         DISEASES   OF   THE   NERVOUS   SYSTEM. 

The  distinction  of  grand  mal  and  the  convulsions  of 
hysteria  is  usually  easy.  In  typical  epileptic  seizures 
there  is  no  apparent  cause  for  the  seizure,  there  is  often 
an  epigastric  or  one-sided  aura,  the  onset  is  abrupt  and 
is  often  accompanied  with  a  cry,  the  seizure  itself  con- 
sists of  tonic  spasm  followed  rapidly  by  clonic  spasm, 
frequently  the  tongue  is  bitten,  the  pupils  are  widely 
dilated,  and  the  face  is  pallid  or  livid  at  the  onset  (an 
important  sign),  micturition  is  common,  the  patient  never 
talks  during  the  seizure,  and  the  duration  of  the  entire 
attack  is  never  more  than  a  few  minutes.  These  features 
contrast  sharply  with  hysteroid  convulsive  seizures,  in 

of  the  relation  which  normally  exists  between  the  preformed  and  the 
combined  or  ethereal  sulphates  in  the  urine  (lo-i).  In  the  cases  to 
which  reference  is  made,  this  relation  is  habitually  changed,  so  that 
there  is  present  an  excessive  proportion  of  the  ethereal  sulphates 
(7-1,  5-1,  or  even  3-1).  The  form  in  which  the  ethereal  sulphates 
occur  in  the  urine  of  such  cases  appears  to  vary  in  different  instances. 
Usually  they  consist  in  large  part  of  indoxyl  sulphate,  which  is  esti- 
mated as  indigo  blue.  In  other  cases  they  may  be  represented  chiefly 
by  phenol  (carbolic  acid).  It  is  not,  of  course,  claimed  that  the  pres- 
ence of  these  substances  is  pathognomonic  of  epilepsy.  They  are 
known  to  occur  in  excess  in  most  cases  of  chronic  Bright's  disease, 
and  probably  occur  in  many  other  states  associated  with  derangement 
of  intestinal  function.  This  circumstance  does  not,  however,  dimin- 
ish the  significance  of  their  presence  in  excess  in  certain  cases  of  epi- 
lepsy, for  it  is  a  striking  fact  that  when  these  substances  are  present 
ihey  bear  a  direct  relation  to  the  occur retice  of  the  paroxysms  ;  i.e., 
though  habitually  present  in  excess  they  become  greatly  increased 
just  before  the  occurrence  of  the  paroxysms,  and  diminish  immedi- 
ately thereafter.  Moreover,  in  some  instances  these  substances  have 
been  diminished  by  means  of  intestinal  antiseptics,  and  so  long  as 
these  have  been  thus  effective,  paroxysms  have  been  staved  off.  It 
has  been  claimed  that  the  occurrence  of  epileptic  paroxysms  is  related 
to  the  defective  elimination  of  uric  acid.  In  a  large  series  of  unpub- 
lished observations  which  bear  upon  this  question,  we  have  found  no 
support  for  this  hypothesis. 


FUNCTIONAL  AND   ORGANIC  DISEASE.         58 1 

which  emotion  commonly  determines  the  attack,  there 
is  no  true  aura^  the  onset  is  not  rarely  gradual,  there  is  no 
cry  at  the  onset,  the  attack  itself  consists  of  periods  of 
prolonged  rigidity,  and  wild,  apparently  purposive,  move- 
ments with  or  without  opisthotonos,  the  pupils  never 
dilate,  micturition  never  occurs,  if  there  is  biting  it  is 
indiscriminate  (hands,  lips,  tongue,  people,  and  things), 
talking  and  groaning  are  common,  and  the  duration  of 
the  attack  is  much  longer  than  in  epilepsy.  In  epilepsy 
the  attack  is  followed  by  stupor  ;  in  hysteria  the  mental 
state  is  clear  immediately  after  the  attack  ceases. 

Nocturnal  attacks  of  grand  mal  may  go  long  unrecog- 
nized. The  most  trustworthy  signs  of  such  attacks  are 
a  feeling  of  soreness  in  the  limbs,  general  headache,  and 
a  sense  of  exhaustion,  minute  hemorrhages  under  the 
skin  of  the  face  and  neck  and  in  the  conjunctivae  (almost 
pathognomonic),  and,  in  adults,  the  occasional  wetting 
of  the  bed.  The  distinction  of  grand  mal  from  the  con- 
vulsions of  uraemia  and  lead  poisoning  depends  on  the 
recognition  of  the  causes  of  the  latter. 

There  is  no  organic  disease  of  the  nervous  system  which 
is  likely  to  be  confounded  with  petit  mal.  The  minor 
attacks  may  generally  be  distinguished  from  attacks  of 
syncope  by  their  sudden  onset  and  termination,  and 
their  occurrence  without  evident  exciting  cause  (such  as 
usually  exists  in  syncope).  Faintness,  dizziness,  or  pal- 
pitation may  occur  in  either  condition  before  the  attack, 
but  the  occurrence  of  a  true  aura  (visual,  olfactory, 
auditory,  visceral)  shows  the  attack  to  be  epileptic. 
Similarly,  slight  mental  confusion  after  the  attack,  mic- 
turition and  slight  rigidity  or  tremor  during  the  attack, 
strongly  suggest  the  epileptic  nature  of  the  seizure. 

A  small  number  of  cases  of  petit  mal  are  distinguished 
by  the  occurrence  of  a  vertiginous  sensation,  and  must 


582         DISEASES   OF   THE  NERVOUS   SYSTEM. 

not  be  confounded  with  true  vertigo.  In  true  vertigo 
there  is  rarely  loss  of  consciousness,  and  the  dizziness 
persists,  while  in  petit  mal  consciousness  is  generally  lost 
or  clouded,  and  the  vertiginous  sensation  passes  quickly 
away.  Aural  vertigo  (due  to  labyrinthine  disease)  {vide 
p.  164.)  can  hardly  be  confounded  with  petit  mal,  if  it  is  re- 
membered that  aural  vertigo  is  characterized  by  persist- 
ent dizziness  after  the  attacks,  tinnitus  aurium,  and  often 
by  persistent  and  defective  hearing,  none  of  which  condi- 
tions occur  in  epilepsy. 

Migraine  (Hemicrania — "  Sick  Headache,"  "  Bilious 
Headache,"  "  Blind  Headache  "). — Migraine  is  a  paroxys- 
mal nervous  disorder  of  which  the  most  characteristic 
feature  is  headache  (often  one-sided).  Nausea  and  vom- 
iting frequently  accompany  the  pain  in  the  head.  In  a 
large  number  of  cases  sensory  disturbances  of  one  kind 
or  another  are  associated  with  the  headache,  and  in  ex- 
ceptional instances  these  sensory  symptoms  are  the  chief 
elements  in  the  paroxysm,  the  headache  being  slight  or 
even  entirely  absent.  Rarely  there  are  motor  disturb- 
ances in  the  limbs  at  the  time  of  the  paroxysms. 

Of  the  sensory  accompaniments  of  migraine  the  most 
important  are  the  disturbances  of  vision,  which  are  pre- 
sent in  some  form  in  more  than  half  the  cases.  These 
manifestations  are  usually  unilateral,  and  consist  in  some 
cases  of  amblyopia,  in  others  of  hemianopsia,  and  in  others 
of  a  bright  moving  spot  on  one  side  of  the  visual  field 
(scintillating  scotoma,  an  early  symptom  of  an  attack). 
The  disturbances  of  speech  v/hich  not  rarely  accompany 
paroxysms  of  migraine  are  usually  of  the  nature  of  sen- 
sory aphasia  (especially  partial  word-deafness).  When 
sensory  phenomena  involve  the  limbs,  they  consist,  like 
the  visual  symptoms,  of  manifestations  of  combined  sen- 
sory irritation  and  sensory  loss  :  there  is  tingling  sue- 


FUNCTIONAL  AND    ORGANIC   DISEASE.  583 

ceeded  by  numbness  and  perhaps  anaesthesia  (fingers 
most  often  involved,  leg  rarely,  always  unilaterally). 
When  motor  symptoms  occur,  they  consist  of  transient 
unilateral  weakness  (arm,  especially  fingers),  and  very 
rarely  of  slight  spasm.  Muscles  supplied  by  the  third 
nerve  are  sometimes  paralyzed  for  a  considerable  period 
(weeks — see  p.  389). 

It  occasionally  happens  that  migraine  is  confounded 
vith  organic  brain  disease.  The  cases  in  which  this  is 
most  likely  to  happen  are  those  in  which  migraine  is  as- 
sociated with  ophthalmoplegia  ("ophthalmic  migraine  "). 
In  these  cases  the  palsy  (always  one-sided,  ptosis, 
strabismus)  comes  on  acutely  with  the  pain  of  migraine, 
but  persists  for  days  or  weeks  with  gradual  improve- 
ment and  ultimate  recovery,  to  recur  at  some  future 
paroxysm  of  migraine.  In  acute  ophthalmoplegia  from 
nuclear  hemorrhage,  the  symptoms  of  hemorrhage 
(apoplexy,  etc.)  are  so  obtrusive  that  no  confusion  can 
occur,  but  from  syphilitic  ophthalmoplegia  the  distinction 
is  not  always  so  easy,  for  the  onset  of  the  palsy  may  be 
rapid  and  attended  with  headache,  and  there  may  be 
spontaneous  recovery  with  subsequent  recurrence  of 
the  symptoms.  The  diagnosis  is  to  be  made  by  close 
attention  to  the  symptoms  and  character  of  the  onset. 
In  migraine  the  palsy  coincides  with  a  paroxysm  which 
is  usually  distinctive  in  character,  and  the  pain  ceases  or 
diminishes  when  the  ophthalmoplegia  comes  on.  In 
syphilitic  ophthalmoplegia  the  palsy  is  never  sudden, 
and  headache  (if  present)  precedes  and  follows  the 
ocular  symptoms. 

Cases  of  migraine  of  the  ophthalmic  variety  appear  to 
be  not  rarely  followed  by  general  paralysis  of  the  insane. 
The  recognition  of  the.  latter  disease  is  sufficiently 
simple  if  its  connection  with  these  cases  of  migraine  be 


584        DISEASES    OF  THE   NERVOUS    SYSTEM. 

known.  The  symptoms  of  ordinary  migraine  recurring 
after  the  onset  of  general  paralysis  may  give  rise  to  error, 
in  that  they  may  be  confounded  with  the  paroxysmal 
attacks  of  that  disease.  Mental  symptoms  resembling 
superficially  the  symptoms  of  general  paralysis  (defec- 
tive memory,  confusion  of  thought,  hesitation  in  speech) 
may  occur  after  severe  paroxysms  of  migraine,  but  are 
distinguished  from  them  by  their  transient  duration  and 
non-progressive  course.  In  most  cases  of  migraine  an 
exciting  cause  can  be  traced  for  each  paroxysm  (over- 
fatigue, dietetic  indiscretion,  ocular  fatigue,  sexual  ex- 
cess, or  several  of  these  factors  combined),  and  this  is 
sometimes  an  aid  in  determining  the  nature  of  a  par- 
oxysm (as  in  the  diagnosis  between  migraine  and  petit 
mal).' 

Chorea. — Chorea  is  a  disease  especially  of  childhood 
and  the  adolescent  period  of  life,  characterized  by  spon- 
taneous spasmodic  and  irregular  movement  (especially 

'  There  are  probably  few  typical  paroxysms  of  migraine  which  are 
not  associated  for  the  time  being  with  evidences  of  disordered  metabo- 
lism. The  nature  of  the  disturbance  seems  to  be  different  in  different 
cases.  The  urine  excreted  just  previous  to  the  paroxysm  is  usually 
highly  concentrated  and  may  contain  a  large  excess  of  phosphoric  acid. 
Whether  there  is  any  abnormality  in  the  excretion  of  uric  acid  in 
migraine,  as  some  have  claimed,  is  as  yet  unsettled.  It  is  improbable 
that  there  is  any  constant  relation  between  uric  acid  excretion  and 
migraine. 

In  one  case  of  recurrent  paroxysmal  vomiting,  perhaps  allied  to  mi- 
graine, there  was  a  striking  diminution  in  the  excretion  of  uric  acid 
during  a  two  days'  period  of  persistent  and  uncontrollable  vomiting. 
In  the  long  intervals  (several  months)  between  the  attacks,  the 
patient,  a  boy  of  eight,  enjoyed  excellent  health,  and  the  relation  be- 
tween the  uric  acid  and  urea  excreted  was  normal  (about  I -60) ; 
during  the  attack  it  was  as  follows:  first  day,  1-159;  second  day, 
1-135.  Immediately  after  the  attack  the  relation  again  became 
normal. 


FUNCTIONAL   AND   ORGANIC   DISEASE.  585 

of  face  and  arm)  and  by  inco-ordination  of  voluntary 
movement.  With  these  symptoms  are  associated  very  fre- 
quently slight  loss  of  power  in  the  parts  affected  by  spasm, 
and  slight,  sometimes  considerable,  mental  change.  We 
have  observed  that  an  excessive  excretion  of  uric  acid 
is  a  highly  constant  condition  in  cases  of  pronounced 
chorea.  In  the  cases  that  have  been  studied  in  relation 
to  this  point  it  has  been  observed  that  the  excretion  of 
uric  acid  has  reverted  to  normal  in  proportion  as  the 
symptoms  have  been  controlled  by  treatment.  In  many 
cases  of  chorea  the  urine  has  a  peculiar  and  rather 
characteristic  red  (somewhat  eosine-like)  color,  probably 
not  due  to  urobilin.  Another*  rather  common  feature 
of  chorea  urines  is  a  diminution  of  the  chlorides  in  rela- 
tion to  the  urea.  Almost  all  chorea  urines  are  of  high 
specific  gravity  (1024-1030)  and  of  very  small  volume  in 
the  twenty-four  hours.  The  disease  is  usually  of  limited 
duration  (six  weeks  to  six  months),  but  occasionally 
lasts  (usually  in  slight  degree)  for  years.  The  chief 
immediate  cause  of  chorea  is  emotion,  especially  fright.' 
The  diagnosis  in  the  large  majority  of  cases  of  chorea 
can  hardly  be  said  to  present  any  difficulties.  In  atypi- 
cal cases  there  is  sometimes  the  possibility  of  confusion 
with  organic   disease.     Thus,   in   those    cases  in  which 

'  The  frequent  association  of  endocarditis  or  rheumatism,  or  both, 
with  chorea,  must  be  borne  in  mind.  The  relation  between  these 
conditions  is  not  understood,  but  it  is  certain  that  this  association  is 
too  frequent  to  be  explained  by  coincidence.  It  seems  probable, 
upon  the  whole,  that  both  the  chorea  and  the  endocarditis  which  pre- 
cedes or  accompanies  it  are  dependent  upon  a  blood-state  identical 
with  or  allied  to  that  of  rheumatism.  The  excessive  excretion  of 
uric  acid  in  chorea,  which  we  have  noted,  is  of  interest  in  this  con- 
nection. The  theory  that  chorea  is  due  to  the  obstruction  (by  emboli 
washed  from  cardiac  valves)  of  the  small  vessels  supplying  the  motor 
structures  of  the  brain  has  little  to  commend  it. 


586        DISEASES   OF   THE   NERVOUS   SYSTEM. 

there  is  considerable  weakness  and  very  little  spasm  an 
organic  cerebral  paralysis  may  be  thought  of.  But  the 
associated  symptoms  of  a  chronic  focal  lesion  (headache, 
optic  neuritis)  are  absent,  the  paralysis  is  limited  to  one 
arm,  and  close  attention  will  show  slight  choreic  spasm 
and  inco-ordination  in  the  affected  limb  and  perhaps  in 
other  parts.  When  the  legs  are  chiefly  affected  in  chorea, 
there  may  be  difficulty  in  walking  and  standing,  but 
confusion  with  spastic  paraplegia  need  not  arise,  for  in 
this  disease  spasm.odic  movements  are  conspicuous  only 
on  voluntary  motion,  and  an  ankle  clonus  is  always 
obtainable. 

Not  very  rarely  the  movements  of  chorea  are  unilateral 
(hemi-chorea),  and  such  cases  may  be  confounded  with 
so-called  "  post-hemiplegic  chorea "  (mobile  spasm, 
athetoid  movements).  These  movements,  however,  are 
usually  slow  (occasionally  they  are  rapid)  and  rhythmical, 
persist  during  sleep,  and  contrast  with  the  quick  irregular 
movements  of  chorea,  which  cease  during  sleep.  There  is 
also  usually  more  or  less  rigidity  in  the  parts  that  are  the 
seat  of  the  post-hemiplegic  movements.  The  history  or 
evidence  of  preceding  hemiplegia  of  course  fixes  the 
diagnosis.  Hysterical  patients  sometimes  develop  true 
chorea  ;  in  other  cases  they  develop  symptoms  which 
while  resembling  chorea  must  be  distinguished  from  it 
(hysterical  chorea).  In  order  to  justify  a  diagnosis  of 
hysterical  chorea  there  must  be  distinct  evidence  that 
the  attack  arose  from  imitation.  The  spasmodic  move- 
ments of  hysterical  chorea  may  be  indistinguishable 
from  those  of  chorea,  but  sometimes  they  have  a  rhyth- 
mical character,  and  often  they  are  more  violent  and 
abrupt  than  those  of  chorea. 

Hereditary  Chorea  (Huntington's  Chorea)  is  an  ob- 
scure form  of  disease  characterized  by  spontaneous  ir- 


FUNCTIONAL  AND   ORGANIC   DISEASE.  587 

regular  spasmodic  movements  resembling  closely  those 
of  ordinary  chorea.  In  other  respects  it  differs  greatly 
from  typical  chorea,  for  it  is  a  disease  especially 
of  adult  life,  is  distinctly  hereditary  (often  through 
several  generations),  and  affects  many  members  of  a 
family,  runs  a  progressive  course,  shows  no  special  re- 
lation to  cardiac  disease  or  to  rheumatism,  never  develops 
from  chorea,  and  is  generally  characterized  by  mental 
failure  and  eventually  by  dementia.  The  disease  is  to  be 
distinguished  from  general  paralysis,  which  it  may  re- 
semble in  its  mental  symptoms,  and  from  bilateral  post- 
hemiplegic atketoid  movements.  From  post-hemiplegic 
disorders  of  movement,  the  absence  of  rigidity  and  the 
irregular  and  wild  character  of  the  movements,  together 
with  the  history,  serve  for  a  distinction.  There  are,  how- 
ever, cases  of  bilateral  athetosis  without  any  history  of  pre- 
ceding acute  cerebral  disease  which  it  may  be  difficult  to 
distinguish  from  hereditary  chorea,  and  which  are  regarded 
by  some  as  possibly  atypical  forms  of  the  latter  disease. 

Paralysis  Agitans  (Parkinson's  Disease — Shak- 
ing Palsy). — Paralysis  agitans  is  a  nutritional  disease 
of  the  central  nervous  system  in  the  second  half  of 
life,  and  is  distinguished  by  the  presence  of  three 
cardinal  symptoms — tremor,  muscular  weakness,  and 
rigidity.  The  disease  is  chronic  and  in  most  instances 
progressive.  The  tremor,  which  is  characterized  by  the 
fact  that  it  continues  during  rest,  usually  precedes  the 
weakness  and  rigidity,  which  come  on  together.  Usually 
the  symptoms  begin  in  the  upper  extremity  (hand),  ex- 
tend to  the  leg  of  the  same  side,  and  if  the  extension 
continues,  to  the  arm  and  then  to  the  leg  of  the  opposite 
side.     The  extension  of  the  disease  is  thus  hemiplegic. 

Typical,  well-marked  cases  of  paralysis  agitans  present 
no    difficulty  in    diagnosis.     Cases    occur,    however,    in 


588        DISEASES   OF  THE  NERVOUS   SYSTEM. 

which  weakness  and  rigidity  of  the  limbs  come  on  with- 
out tremor  and  without  the  characteristic  attitude  and 
facial  expression  of  paralysis  agitans,  namely,  a  bending 
forward  of  the  head  and  upper  part  of  the  spine  and  a 
fixed  anxious  expression.  If  in  such  cases  there  is  con- 
siderable mental  weakness,  the  diagnosis  from  organic 
brain  disease  may  be  difficult  until  the  appearance  of 
tremor.  An  important  point  of  distinction  from  slight 
hemiplegia  is  that  the  knee-jerks  are  not  increased  on 
one  side  as  in  hemiplegia. 

The  legs  are  sometimes  chiefly  affected  in  paralysis 
agitans,  and  in  such  cases  the  suspicion  of  spinal  cord 
disease  may  arise,  but  will  be  dispelled  by  the  detection 
of  slight  tremor  in  the  arms  and  by  the  fixity  of  gaze. 

The  diagnosis  from  insular  sclerosis  is  always  easy  if 
the  following  facts  be  remembered  :  In  insular  sclerosis 
the  tremor  occurs  only  on  movement  (intention  tremor), 
and  is  wider  in  range  and  more  irregular  than  that  of 
paralysis  agitans.  Insular  sclerosis  rarely  commences 
after  forty,  paralysis  agitans  rarely  before  thirty.  The 
head  is  regularly  involved  in  the  tremor  of  insular  sclero- 
sis; in  paralysis  agitans  it  is  only  occasionally  affected. 
Nystagmus  is  usually  present  in  insular  sclerosis;  in 
paralysis  agitans  it  never  occurs.  The  speech  disturb- 
ances of  the  two  diseases  are  different.  In  paralysis  agi- 
tans the  voice  is  monotonous  and  without  emotion  and 
expression,  and  the  words  are  often  run  together;  in  in- 
sular sclerosis  the  syllables  are  unduly  separated  as  a  rule. 
The  fundus  is  normal  in  paralysis  agitans;  in  insular  scle- 
rosis there  is  often  slight  ophthalmoscopic  change  (slight 
optic  nerve  atrophy).  Furthermore,  the  peculiar  atti- 
tude, fixity  of  facial  expression,  and  muscular  rigidity  of 
paralysis  agitans  are  all  absent  in  insular  sclerosis. 

Post-hemiplegic  tremor  is  fine,  while  the  tremor  of  par- 


FUNCTIONAL  AND   ORGANIC   DISEASE. 


589 


alysis  agitans  is  coarse.  In  post-hemiplegic  tremor  the 
carriage  and  facial  expression  are  normal  and  a  history 
of  hemiplegia  is  usually  available.  These  points  serve 
to  prevent  error  in  diagnosis. 

Paralysis  agitans  is  to  be  distinguished  from  "senile 
tremor,"  a  fine  tremor  of  the  limbs  and  head  which  is 


FIG.  66. 
Paralysis  agitans.     (After  St.  Leger.)    (Gowers.) 

seen  in  many  aged  persons.  The  tremor  is  finer  than 
that  of  paralysis  agitans,  affects  the  head  early,  involves 
both  upper  extremities  about  the  same  time  and  is  un- 
associated  with  the  rigidity  which  is  so  characteristic  a 
feature  of  paralysis  agitans.  These  features  serve  for  a 
distinction  from  paralysis  agitans,  but  there  are  cases 


590  DISEASES   OF  THE   NERVOUS   SYSTEM. 

intermediate  in  character  between  the  two  conditions 
which  it  is  impossible  to  classify. 

Neuralgia. — The  word  neuralgia  is  merely  a  euphe- 
mism for  nerve-pain,  and  nerve-pain  may  occur  under  two 
very  different  conditions,  namely,  as  the  result  of  struc- 
tural irritative  disease  of  a  nerve,  and  as  the  result  of 
purely  nutritional  changes  in  a  nerve  without  any  demon- 
strable alterations  in  its  structure.  It  is  eminently  de- 
sirable that  the  word  neuralgia  should  be  restricted  to 
that  form  of  nerve-pain  in  which  there  is  no  structural 
disease  of  the  affected  nerve  or  nerves — "idiopathic" 
neuralgia.  The  form  of  nerve-pain  that  depends  on 
structural  disease  ("  symptomatic  neuralgia  ")  should  be 
referred  to  the  process  which  is  its  usual  cause,  namely, 
neuritis. 

While  the  distinction  of  these  two  forms  of  nerve-pain 
is  thus  clear  in  theory,  it  is  by  no  means  always  easy  in 
practice.  They  possess  many  features  in  common,  and 
their  successful  separation  involves  an  accurate  knowl- 
edge of  the  diagnostic  characters  of  each  form. 

The  chief  diagnostic  features  of  typical  neuralgia  are 
as  follows  :  (i)  the  unilateral  distribution  of  the  pain  ; 
(2)  its  distinctly  paroxysmal  character  ;  (3)  changes  in 
the  position  of  the  pain  ;  (4)  the  absence  of  all  evidences 
of  organic  disease  of  the  nerve  involved  (absence  of  local 
tenderness  and  swelling  of  nerve  where  the  nerve  is  ac- 
cessible). 

In  some  cases  of  neuralgia  the  pain  is  not  migratory, 
but  fixed.  Such  neuralgia  must  be  distinguished  both 
from  the  fixed  pain  of  pressure  neuritis  and  from  that 
of  slight  spontaneous  neuritis.  Where  the  nerve-pain 
depends  on  pressure  (bone  disease,  tumor),  there  are 
almost  certainly  other   symptoms  of  such  pressure,  and 


FUNCTIONAL  AND    ORGANIC   DISEASE.  59 1 

the  pain  steadily  progresses  in  intensity  and  suggests  its 
dependence  on  a  progressive  cause. 

The  pain  of  neuralgia  is  sometimes  indistinguishable 
from  that  of  slight  neuritis.  Usually,  however,  a  dis- 
tinction can  be  made  and  is  based  on  the  following  facts  : 
(i)  the  pain  of  neuritis  is  continuous  or  nearly  so  ;  (2) 
changes  in  the  sensibility  of  the  skin  supplied  by  the 
nerve  are  apt  to  be  present  and  are  persistent  in  charac- 
ter (hyperaesthesia,  anaesthesia);  (3)  if  the  affected  nerve 
is  a  "mixed  "  nerve,  the  muscles  which  it  supplies  become 
flabby,  and  their  irritability  to  galvanism  and  faradism  is 
at  first  slightly  increased;  (4)  there  are  often  slight  trophic 
changes  in  the  skin  ;  (5)  if  the  nerve  is  accessible  it  is 
usually  tender  to  pressure  and  often  swollen.  Of  course 
the  mere  absence  of  nerve  tenderness  and  swelling  does 
not  exclude  neuritis.  On  the  other  hand  the  presence 
of  transient  tenderness  at  the  time  of  the  pain  paroxysm 
does  not  mean  neuritis,  for  such  tenderness  is  common  in 
neuralgia.  It  is  only  where  local  tenderness  exists  both 
at  the  time  of  the  paroxysm  and  in  the  intervals,  and  is 
present  early  in  the  affection  (within  the  first  few  weeks), 
that  it  can  be  regarded  as  a  certain  indication  of  neuritis. 

When  the  indications  as  to  the  nature  of  the  nerve  pain 
are  equivocal  the  history  of  the  case  may  be  allowed 
weight.  Thus  the  fact  that  the  patient  has  been  a 
sufferer  from  nerve  pains  in  other  parts  makes  the  neu- 
ralgic nature  of  the  affection  probable.  The  etiological 
factors  may  also  be  given  some  importance.  Thus,  a 
family  history  of  neuralgia  or  of  functional  nervous 
disease,  a  history  of  a  period  of  general  debility  before 
the  development  of  the  pain,  or  a  knowledge  of  the  fact 
that  the  nerve  pains  are  often  related  to  mental  influences, 
would  each  of  them  increase  the  probability  that  the 
trouble  was  functional  and  not  organic. 


592         DISEASES   OF  THE   NERVOUS   SYSTEM. 

Various  organic  affections  of  the  nervous  system  are 
apt  to  be  confounded  with  neuralgia.  We  may  touch 
briefly  upon  some  of  the  errors  in  diagnosis  that  are 
especially  liable  to  arise. 

In  caries  of  the  upper  cervical  vertebrae,  there  are 
often  severe  neuralgiform  pains  in  the  region  of  the  greater 
and  lesser  occipital  nerves  during  the  early  stage  of  the 
disease.  Usually  the  pain  is  one-sided.  The  distinction 
of  these  cases  from  cervico-occipital  neuralgia  may  cause 
some  difficulty  unless  it  be  borne  in  mind  that  the  pain  of 
caries  is  aggravated  by  motion  or  jarring  and  that  such 
pain  is  associated  with  spasm  in  the  deep  cervical  muscles 
on  the  side  of  the  pain. 

Neuralgiform  pains  are  common  in  disease  of  the  ab- 
dominal and  thoracic  viscera.  Whenever,  therefore,  there 
is  unilateral  neuralgic  pain  in  the  trunk,  a  careful  physical 
examination  must  be  made  of  the  organs  near  the  seat  of 
pain.  In  some  cases  of  thoracic  disease  the  pain  does 
not  correspond  to  the  seat  of  the  disease,  but  is  "  reflected  " 
to  distant  parts.  Thus  an  aneurism  of  the  aorta  may  cause 
little  local  pain,  but  may  give  rise  to  severe  neuralgiform 
pain  in  the  arm.  In  ordinary  intercostal  neuralgia  there 
are  tender  points  at  certain  characteristic  situations  in 
the  course  of  the  nerve — at  a  point  corresponding  to  the 
emergence  of  the  nerve  from  the  intervertebral  foramen, 
at  a  point  near  the  middle  line  in  front,  and  at  a  point  in 
the  axillary  region  about  midway  between  these.  These 
points  of  tenderness  are  seldom  found  in  the  neuralgias  from 
disease  of  internal  organs.  The  "  lightning  pains  "  of 
tabes  are  sometimes  experienced  in  the  trunk,  especially 
in  its  lower  part.  These  pains  are,  however,  of  such  short 
duration  and  so  shifting  in  seat  that  they  are  not  likely 
to  be  confounded  with  neuralgia.  Moreover,  they  are 
associated  usually  with  pains  in  the  legs,  with  disturbances 


FUNCTIONAL  AND   ORGANIC  DISEASE.         593 

of  sensibility,  and,  usually,  with  loss  of  knee-jerk  or  loss 
of  the  light-reflex  of  the  iris. 

The  trunk  may  be  the  seat  of  severe  neuralgiform  pains 
in  the  early  stage  of  a  tumor  of  the  spinal  cord.  The 
severity  and  constancy  of  these  pains  are  their  character- 
istic features,  and  should  always  excite  suspicion  of  organic 
disease.  Moreover,  the  pain  is  usually  increased  by  a 
lateral  or  rotary  movement  of  the  spine,  a  feature  most 
suggestive  of  organic  disease.  In  the  cases  where  there 
is  evidence  of  pressure  upon  the  cord,  there  is,  of  course, 
no  diagnostic  difficulty,  but  it  often  happens  that  the 
neuralgiform  pains  precede  the  development  of  such 
symptoms  by  a  considerable  period.  In  disease  of  the  ver- 
tebral column  there  is  often  intense  unilateral  pain,  but 
this  pain  is  usually  much  increased  by  any  movement  of 
the  trunk. 

The  diagnosis  of  sciatica  may  conveniently  be  con- 
sidered here.  The  term  sciatica  is  applied  to  any  con- 
dition characterized  by  pain  in  the  region  of  the  sciatic 
nerve,  whether  the  pain  be  due  to  a  primary  affection  of 
the  nerve,  or  whether  it  depends  on  damage  to  the  nerve 
from  causes  outside  it.  It  is  well  to  restrict  the  word  to 
the  primary  affections  of  the  nerve,  sciatic  neuralgia  and 
sciatic  neuritis.  The  chief  point  of  distinction  between 
sciatic  neuralgia  and  sciatic  neuritis  is  that  in  the  latter 
condition  there  is  persistent  tenderness  of  the  sciatic 
nerve. 

The  pain  of  sciatica  is  sometimes  felt  near  the  hip- 
joint,  but  it  is  almost  impossible  to  confound  the  pains 
of  hip-disease  with  those  of  sciatica.  In  sciatica  the  pain 
extends  far  down  the  thigh  in  the  line  of  the  sciatic  nerve, 
and  is  increased  in  this  distribution  when  the  nerve  is 
put  on  the  stretch,  and  there  is  usually  some  tenderness 
(at  least  at  times)  in  the  nerve.   When  sciatic  pain  is 


594        DISEASES   OF   THE   NERVOUS   SYSTEM. 

secondary  to  pressure  on  the  sacral  plexus  by  pelvic  or 
abdominal  tumors  there  is  usually  little  tenderness  of  the 
nerve  in  proportion  to  the  degree  of  pain  referred  to  it. 
This  condition  should  excite  suspicion  of  organic  pelvic 
disease  and  lead  to  a  rectal  examination.  It  is  important 
to  remember  that  primary  sciatica  is  practically  never 
bilateral.. 

Primary  neuralgia  in  the  distribution  of  the  anterior 
crural  nerve  is  rare.  Neuralgiform  pain  in  this  situation 
is  likely  to  depend  on  pressure  upon  the  lumbar  plexus,  or 
upon  neuritis  of  this  plexus  secondary  to  a  sciatic  neuritis. 
In  either  case  there  is  some  wasting  of  the  anterior  thigh 
muscles  and  slight  or  considerable  changes  in  their  elec- 
trical irritability.  In  many  cases  there  is,  moreover,  loss 
of  knee-jerk.  None  of  these  conditions  are  ever  present 
in  neuralgia. 

Occupation  Neuroses. — It  is  here  convenient  to 
touch  very  briefly  on  the  diagnosis  of  that  class  of  affec- 
tions which  is  characterized  by  the  occurrence  of  certain 
motor  and  sensory  symptoms  (especially  spasm  and  pain) 
as  the  consequence  of  frequently  repeated  muscular  acts 
appertaining  usually  to  the  occupation  of  the  patient. 

The  most  important  general  characters  of  these  "  occu- 
pation neuroses,"  as  they  are  called,  are  as  follows  :  (i) 
The  symptoms  above  referred  to  occur  in  the  part  which 
is  concerned  in  the  habitual  muscular  action.  (2)  This 
habitual  muscular  action  is  interfered  with  and  perhaps 
effectually  prevented  by  the  symptoms.  (3)  The  most 
common  symptom  is  spasm  in  the  parts  affected 
("cramp";  hence  "writer's  cramp,"  "telegraphist's 
cramp,"  etc.).  (4)  With  this  spasm,  or  unassociated  with 
it,  occurs  pain,  referred  to  the  muscles,  bones,  joints,  or 
nerves,  and  excited,  at  first ^  only  by  the  special  muscular 
action. 


FUNCTIONAL  AND   ORGANIC   DISEASE.  595 

The  chief  forms  of  occupation  neuroses  are  the  follow- 
ing :  Writer's  cramp,  piano-forte  player's  cramp,  teleg- 
raphist's cramp,  needle-women's  cramp,  and  violin  play- 
er's neurosis.  But  almost  any  occupation  that  involves 
often  repeated  special  muscular  acts  occasionally  makes  a 
victim  of  an  occupation  neurosis.  In  most  cases  of  oc- 
cupation neurosis  there  is  a  combination  of  spasm  and 
pain  ;  but  very  often  one  of  these  symptoms  predomi- 
nates, and  it  is  accordingly  convenient  to  distinguish  a 
motor  or  spasmodic  form  and  a  sensory  or  neuralgic  form 
of  occupation  neurosis. 

The  occupation  neuroses  seldom  occur  in  persons  in 
perfect  health.  They  develop  usually  in  persons  who 
have  become  debilitated  from  some  cause,  and  are  dis- 
tinctly neurasthenic.  Often  a  neuropathic  heredity  can 
be  traced.  A  period  of  anxiety  not  rarely  precedes  the 
development  of  the  neurosis,  and  sometimes  its  develop- 
ment is  related  to  a  local  disease  or  injury.  It  seems 
probable  that  these  varied  influences  operate  by  produ- 
cing a  functional  derangement  in  the  nervous  centres 
(especially  the  cerebral  centres)  concerned  in  the  par- 
ticular act  whose  frequent  repetition  has  excited  the  local 
affection. 

The  diagnosis  of  the  occupation  neurosis  is  not  usually 
difficult.  The  relation  between  a  given  affection  and  the 
action  on  which  it  depends  is  generally  sufficiently  obtru- 
sive. In  the  case  of  the  most  common  of  these  neuroses 
— writer's  cramp — confusion  may  at  times  arise  with 
paralytic  affections  (chiefly  hemiplegia  of  gradual  onset) 
in  which  the  interference  with  writing  is  thought  to  de- 
pend on  the  neurosis.  Knowledge  of  one  fact  suffices  to 
make  the  distinction  of  writer's  cramp  from  all  other 
forms  of  disease.  It  is  this  :  In  writer's  cramp  the  symp- 
toms are  at  first  brought  on  only  by  the  act  of  writing.     In 


59^3       DISEASES    OF   THE    NERVOUS    SYSTEM. 

all  other  affections  (paralysis,  paralysis  agitans,  tremors, 
etc.),  the  symptoms  are  not  limited  to  the  act  of  writing, 
but  may  be  observed  in  all  other  acts  that  require  the  use 
of  the  affected  parts.  This  diagnostic  feature  applies, 
mutatis  mutandis,  to  the  diagnosis  of  the  less  common 
forms  of  occupation  neuroses. 

Delirium  Tremens  (Acute  Alcoholism,  Alcoholic  De- 
lirium).— Delirium  tremens  is  an  acute  nutritional  affec- 
tion of  the  brain,  involving  especially  the  nerve-elements 
of  the  cortex.  The  disease  runs  a  definite  course,  and 
has  a  strong  tendency  to  subside  spontaneously.  It  is 
practically  confined  to  drunkards,  and  usually  follows  a 
prolonged  "  spree." 

The  symptoms  of  delirium  tremens  are  of  rather  rapid 
development  and  usually  attain  their  full  development  in 
the  course  of  a  few  days.  The  early  symptoms  are  par- 
tial insomnia,  bad  dreams,  restlessness,  mental  depression, 
and  loss  of  appetite.  When  the  symptoms  are  fully  de- 
veloped, there  are  distressing  and  rather  characteristic 
hallucinations  and  illusions,  especially  of  sight,  both  at 
night  and  during  the  day.  Very  often  the  patient  sees 
snakes  or  spiders  crawling  on  his  bed  or  on  the  walls,  or 
sees  grinning  faces  of  men  or  devils.  The  false  sense 
impressions  give  rise  to  delusions  of  a  fearful  character. 
Associated  with  this  mental  condition  is  a  characteristic 
irregular  tremor  of  rather  wide  range,  which  occurs  on 
movement.  The  temperature  is  almost  always  elevated, 
the  degree  of  fever  being  proportioned  to  the  severity  of 
the  disease. 

The  diagnosis  of  delirium  tremens  seldom  presents  any 
difficulty.  From  acute  meningitis  it  is  distinguished  by 
the  absence  of  headache,  spasm,  and  paralysis.  From 
ordinary  symptomatic  delirium  it  is  readily  distinguished 
by  the  great  prominence  of  the  terrifying  visual  halluci- 


FUNCTIONAL  AND   ORGANIC   DISEASE.  59; 

nations  and  by  the  presence  of  tremor.  Sometimes  de- 
lirium tremens  is  confounded  with  general  paralysis  of 
the  insane  or  with  acute  mania.  The  horrifying  halluci- 
nations of  delirium  tremens  cannot  be  mistaken  for  the 
exalted  mental  and  physical  activity  of  acute  mania. 
The  characteristic  irregular  tremor  of  delirium  tremens  is 
absent  in  acute  mania.  Considerable  irregular  tremor 
may,  however,  occur  in  general  paralysis  ;  but  the  busy 
anxiety  and  visual  hallucinations  of  alcoholic  delirium 
make  a  strong  contrast  with  the  unnatural  complacency 
and  delusions  of  grandeur  that  characterize  the  organic 
cerebral  affection. 

Cerebral  Concussion. — A  certain  degree  of  cerebral 
concussion  is  an  accompaniment  of  many  forms  of  injury 
to  the  head,  and  its  symptoms  are  then  lost  in  those  of 
the  trauma.  Numerous  cases  occur,  however,  in  which 
the  only  symptoms  are  such  as  must  be  referred  to  violent 
concussion  of  the  brain.  It  is  probable  that  in  some  of 
these  cases  of  violent  concussion  the  symptoms  depend, 
in  part  at  least,  on  the  occurrence  of  minute  foci  of 
hemorrhage  into  the  substance  of  the  brain  (sub-cortical 
white  substance,  sometimes  mid-brain  and  pons).  This 
fact  removes  these  cases  from  the  category  of  strictly 
functional  disease,  but  the  character  of  the  symptoms  is 
such  as  suggests  functional  rather  than  organic  disease, 
and  justifies  their  consideration  here. 

The  symptoms  of  cerebral  concussion  vary  much.  The 
blow  or  fall  which  causes  the  concussion  gives  rise  almost 
immediately  to  loss  of  consciousness,  or  to  a  confused 
mental  state.  In  some  cases  the  loss  of  consciousness  is 
associated  almost  immediately  with  irritative  phenomena 
of  a  cortical  nature — unilateral  and  bilateral  clonic  spasm, 
increased  reflex  irritability,  increase  in  myotic  irritability, 
and  often  ankle  clonus.    The  pupils  are  often  contracted, 


59S         DISEASES   OF   THE   NERVOUS   SYSTEM. 

the  pulse  is  slowed,  and  there  may  be  repeated  vomiting. 
Nystagmus  is  a  common  symptom.  It  is  often  very  rapid, 
and  the  oscillations  may  be  vertical  as  well  as  horizontal. 
Rapidly  changing  strabismus  often  occurs  ;  internal  stra- 
bismus alternates  with  external  strabismus.  In  young 
children  nystagmus,  rotary  spasm  of  the  muscles  of  the 
neck,  and  strabismus  often  follow  relatively  slight  con- 
cussions (falls  from  chairs  or  cribs)  without  loss  of 
consciousness.  These  irritative  symptoms  are  usually  of 
short  duration  (few  hours  or  days),  and  gradually  wear 
away.  In  adults  cerebral  symptoms  may  persist  for 
several  weeks  (headache,  mental  confusion,  slight  spasm, 
slow  pulse).  Afrslight  elevation  of  temperature  occurs  in 
some  cases  and  lasts  several  days. 

The  diagnosis  from  organic  disease  is  not  always  easy 
if  the  history  of  a  concussion  is  not  known.  The  irri- 
tative symptoms  (unilateral  and  general  spasm,  strabis- 
mus, vomiting,  slow  pulse,)  and  slight  fever  may  suggest 
meningitis.  The  spasm  in  concussion  is  often  more 
violent  than  that  of  meningitis,  and  more  continuous.  The 
symptoms  are  also  more  rapidly  changeable.  In  short, 
the  irritative  symptoms  are  more  intensely  acute.  In 
concussion  the  symptoms  come  on  immediately  after  the 
injury  and  reach  their  maximum  in  a  short  time.  They 
also  rapidly  subside.  In  meningitis  the  symptoms  more 
slowly  reach  their  maximum,  there  is  more  fever,  and  de- 
lirium precedes  stupor.  When  the  irritative  symptoms 
are  not  so  marked,  there  may  be  a  just  suspicion  of  com- 
mencing meningitis  for  several  days.  Thus  headache,  som- 
nolence, mental  confusion,  slight  fever,  a  slow  pulse,  and 
slight  spasm  may  last  many  days  after  a  concussion,  and 
then  gradually  clear  up. 

It  is  exceedingly  important  to  distinguish  between 
cerebral  concussion  and  extradural  hemorrhage.       The 


FUNCTIONAL  AND   ORGANIC   DISEASE.  599 

two  conditions  may  co-exist.  The  distinction  rests  chiefly 
on  the  fact  that  in  extradural  hemorrhage  there  are 
distinct  evidences  of  hemiplegia  with  or  without  spasm, 
while  in  concussion,  paralysis,  if  present,  is  slight,  and  on 
the  fact  that  the  symptoms  of  extradurul  hemorrhage  are 
preceded  by  a  lucid  interval,  and  do  not  come  on  sud- 
denly. In  extradural  hemorrhage,  again,  there  is  usually 
evidence  of  fracture. 

In  young  children,  the  significance  of  nystagmus,  or 
rotary  spasm  and  nystagmus,  following  immediately  on 
an  injury  is  sufficiently  plain. 

Malingering. — Malingering  is  the  simulation  of  a 
morbid  condition  which  has  no  basis  whatever  in  fact, 
and  in  the  case  of  nervous  diseases  is  not  very  un- 
common. Malingering  must  be  carefully  distinguished 
from  the  mere  exaggeration  of  a  morbid  condition,  which 
is  very  common  indeed,  especially  in  hysterical  con- 
ditions. 

Many  cases  of  malingering  are  so  patent  that  they 
would  not  impose  on  a  novice,  others  require  much 
patience  and  knowledge  for  their  detection,  and  others 
still  may  deceive  the  best  educated  physician.  The  at- 
tempt to  feign  organic  disease,  or  diseases  with  decidedly 
objective  signs,  is  not  very  common,  and  need  never  be 
successful.  But  functional  diseases,  of  which  the  symp- 
toms are  chiefly  subjective,  are  often  successfully  simu- 
lated. Thus  pain  of  every  variety  and  distribution  may 
be  successfully  feigned,  but  it  is  more  difficult  to  feign 
convulsive  seizures  or  paralysis.  There  is  good  reason 
to  think  that  loss  of  sensibility  to  pain  may  be  so  suc- 
cessfully simulated,  even  under  the  severest  tests  by  the 
faradic  brush,  the  needle,  etc. 

In  any  case  where  malingering  is  suspected,  especial 
attention  should  be  given  the  objective  signs   that  may 


600         DISEASES   OF   THE  NERVOUS   SYSTEM. 

exist,  for  the  purpose  of  comparing  these,  as  regards  de- 
tail and  grouping,  with  forms  of  actual  disease  which 
they  resemble.  Close  attention  will  always  reveal  im- 
portant though  perhaps  slight  differences.  Thus  while 
a  malingerer  may  imitate  closely  the  character  of  seizures 
of  grand  mal,  examination  at  the  beginning  of  the  paroxysm 
will  show  that  the  vaso-motor  symptoms — facial  pallor  and 
dilatation  of  the  pupil — do  not  occur.  An  almost  universal 
tendency  is  for  malingerers  to  overdo  their  part — both 
in  the  feigning  of  objective  symptoms  and  in  complaints 
about  subjective  states. 

But  while  a  diagnosis  may  often  be  made  from  the 
symptoms  themselves,  it  is  commonly  desirable  or  neces- 
sary to  obtain  information  from  other  sources.  The 
history  of  the  patient  should  be  obtained  with  regard 
especially  to  his  character,  his  social  and  his  financial 
condition.  It  is  especially  important  to  know  what 
incentive  there  may  be  for  malingering,  whether,  for 
example,  in  alleged  traumatic  cases,  the  patient  expects 
to  recover  damages  (as  in  railroad  cases),  whether  the 
patient  is  poor  and  shiftless  or  independent  and  thrifty. 
An  exceedingly  important  thing,  where  elaborate  ma- 
lingering is  suspected,  is  to  find  out  whether  the  patient 
has  had  opportunities  for  the  observation  of  the  symptoms 
of  nervous  diseases,  whether  he  has  lived  in  hospitals,  or 
has  been  about  from  dispensary  to  dispensary,  and  has 
been  repeatedly  examined  for  nervous  symptoms.  Thus 
some  symptoms,  as  hemianaesthesia,  hemianopsia,  re- 
striction of  the  visual  field,  etc.,  are  not  likely  to  be 
feigned,  but  may,  nevertheless,  be  successfully  feigned 
by  an  intelligent  patient  who  has  discovered,  by 
experience  at  hospitals  and  dispensaries,  the  significance 
attached  to  these  signs.  A  single  unequivocal  symptom 
or  sign  of  organic  disease  should  be  allowed  great  weight 


FUNCTIONAL  AND    ORGANIC   DISEASE.         6oi 

if  found.  Of  such  symptoms  and  signs  the  most  im- 
portant are  local  muscular  atrophy,  changes  in  electrical 
reaction  (RD),  ankle  clonus,  increase  or  loss  of  knee- 
jerk  on  one  side,  slight  optic  neuritis  or  atrophy,  incon- 
tinence of  urine  or  faeces,  and  paralysis  of  cranial  nerves. 
Insomnia  is  a  symptom  which  cannot  long  be  successfully 
feigned.  Its  persistence  when  the  patient  believes  him- 
self to  be  free  from  observation  is  significant  of  at  least 
functional  disturbance. 

When  the  symptoms  of  actual  disease,  functional  or 
organic,  are  exaggerated  by  a  patient,  it  is  exceedingly 
difficult  to  estimate  the  degree  of  exaggeration,  unless  this 
be  very  extreme.  A  close  watch  for  feigned  symptoms 
for  a  considerable  period  of  time  may  furnish  data  for 
the  estimation  of  the  degree  of  exaggeration,  but  there 
are  many  cases  in  which  the  best  observers  would  differ 
in  their  judgment  on  this  point. 


CHAPTER   VII. 

EXAMINATION    OF    THE    PATIENT. 

In  the  clinical  study  of  nervous  diseases  it  is  essential 
for  accuracy  and  rapidity  in  diagnosis  to  employ  a  sys- 
tematic method  of  examining  patients. 

Inasmuch  as  the  forms  of  nervous  diseases  vary  so 
much  in  character,  no  one  method  of  examination  can 
always  be  adhered  to  rigidly,  but  this  does  not  destroy 
the  feasibility  of  using  a  more  or  less  definite  system  of 
study  of  the  cases.  In  the  following  pages  a  general 
method  of  procedure  is  indicated  which  may  be  modified 
or  curtailed  to  suit  individual  diseases.  When  a  patient 
is  first  seen  by  the  physician  it  is  often  eminently  desir- 
able to  make  a  preliminary  rapid  survey  of  the  case. 
Such  examination  sometimes  enables  the  physician  to 
make  a  provisional  diagnosis  for  immediate  treatment 
and  gain  intelligent  guidance  for  subsequent  more 
elaborate  and  special  examination.  A  preliminary  ex- 
amination should  cover  the  essential  points  of  an  ex- 
tended scheme;  a  detailed  record  of  the  latter  is  shown 
in  a  composite  case  which  is  reproduced  here  to  illus- 
trate the  points  in  the  examination.  In  recording  the 
clinical  findings  of  the  examination  intelligible  abbrevia- 
tions should  be  used  wherever  possible,  but  the  use  of 
symbols  is  to  be  discouraged  for  obvious  reasons. 

The  diagnosis  must  rest  largely,  at  least  in  most  cases, 

602 


EXAMINATION   OF  THE   PATIENT.  603 

upon  the  careful  objective  or  direct  examination  of  the 
patient  for  the  detection  of  the  signs  and  symptoms  of 
disease.  The  history  of  the  patient  and  of  the  develop- 
ment of  his  disease  as  gathered  from  the  patient  or  his 
friends  is  of  course  of  great  importance,  but  the  diag- 
nostic indications  that  are  obtained  in  this  way  are  to  be 
used  in  subordination  to  the  objective  signs  of  disease 
about  to  be  detailed.  Where  the  indications  derived 
from  the  two  sources  conflict,  preference  is  always  to  be 
given  to  conclusions  that  are  obtained  from  an  examina- 
tion of  the  patient.  In  short,  an  effort  should  constantly 
be  made  to  make  the  diagnosis  of  organic  nervous  dis- 
eases as  purely  objective  as  possible,  the  history  being 
used  chiefly  in  subordination  to  the  physical  signs  for  the 
confirmation  and  correction  of  the  diagnosis  based  upon 
them. 

The  history  properly  begins  with  a  concise  statement 
of  the  most  obtrusive  subjective  symptoms  and  their 
duration:  in  short,  the  main  symptoms  of  which  the 
patient  complains. 

The  Family  History  should  contain  the  cause  of  death 
of  the  patient's  immediate  relatives,  particularly  as  re- 
gards the  influence  of  alcohol,  syphilis,  tuberculosis,  in- 
sanity, epilepsy  or  other  nervous  diseases  in  the  parents. 

The  Personal  History  should  be  taken  and  recorded  in 
the  chronological  order  as  far  as  possible,  beginning 
with  the  patient's  intra-uterine  life,  birth,  the  accidents 
and  morbid  incidents  attending  the  same,  diseases  of 
infancy,  habits,  etc.  Evidence  of  infantile  rickets  should 
be  carefully  searched  for  as  they  often  play  an  important 
role  in  deciding  the  vulnerability  of  an  individual  to 
nervous  disease  in  after  life,  particularly  as  to  degenera- 
tive diseases,  such  as  epilepsy  and  allied  conditions. 

Present  Illness. — Data  relating  to  the  present  illness 


6o4        DISEASES   OF  THE   NERVOUS   SYSTEM. 

should  also  be  arranged  in  the  chronological  order  of 
their  occurrence,  following  which  a  short  resume  of  the 
present  condition  or  status  of  the  patient  should  be  given. 
It  should  include  both  the  physical  and  mental  state. 
The  principal  neurological  facts  of  a  mental  inquiry  con- 
cern states  of  alienation,  exaltation,  perversion,  depres- 
sion or  defect,  and  whether  there  be  stupor,  delirium 
or  coma.  The  state  of  memory,  the  presence  of  vertigo, 
convulsions,  headache,  epileptic  or  apoplectic  attacks, 
vomitings,  etc.,  should  all  be  inquired  into. 

The  Physical  Examination  is  begun  by  examining  the 
sensory  and  motor  functions  of  the  cranial  nerves; 
this  is  done  by  taking  each  one  in  its  numerical 
order. 

I.  Olfactory. — Inasmuch  as  a  loss  of  the  sense  of 
smell  is  less  frequently  due  to  a  lesion  of  the  nerve  than 
to  disease  of  the  mucous  membrane,  the  latter  cause 
must  be  first  excluded.  Persons  who  have  lost  the 
sense  of  smell  often  complain  of  a  loss  of  taste  only,  as 
that  is  the  more  serious  deprivation.  In  testing  this 
sense  substances  such  as  assafoetida,  musk,  peppermint 
and  cloves  should  be  employed,  as  they  act  on  the  sense 
of  smell  only;  moreover  they  are  easily  identified  and 
named.  Only  a  small  portion  of  the  testing  substance 
should  be  used  on  the  bottle  stopper  or  on  a  piece  of 
cotton  wool  and  applied  only  for  a  short  time  as  exces- 
sive stimulation  may  deaden  or  paralyze  a  weakened  or 
imperfect  sense  before  the  entire  examination  is  finished. 
The  test  should  be  applied  to  either  nostril  alternately, 
the  patient  being  required  to  recognize  and  name  the 
test  substance.  Many  persons,  even  though  such  com- 
mon substances  as  here  mentioned  be  employed,  are 
able  to  recognize  only  an  odor  without  naming  it,  but 
practical   ends    will   be    subserved  if   this   be   so,  as  a 


EXAMINATION   OF   THE   PATIENT.  605 

knowledge  that  the  nerve  impulses  are  transmitted  is 
quite  sufficient. 

II.  Optic  Nerve. — The  examination  of  the  optic  nerve 
is  restricted  from  a  neurological  view-point  to  {a)  test  of 
the  acuteness  of  vision,  {fi)  the  fields  of  vision,  {/)  state 
of  the  optic  disc.  The  acuteness  is  tested  either  for  dis- 
tant or  near  vision,  or  both,  the  former  by  the  use  of 
Snellen's  test  type  at  a  distance  of  twenty  feet  (six 
metres)  since  rays  of  light  from  that  distance  are  practi- 
cally parallel.  The  acuteness  of  vision  is  expressed  by 
a  fraction,  the  numerator  of  which  corresponds  to  the 
number  of  feet  separating  the  patient  from  the  chart 
(twenty),  and  the  denominator  to  the  number  indicating 
the  distances  at  which  the  smallest  letters  seen  should 
be  read  by  the  normal  eye.  Thus  if  the  patient's  sight 
is  normal,  his  acuteness  of  vision  will  equal  f^;  this 
would  be  expressed  for  the  right  eye  R  V  =  \%.  If 
vision  is  less  than  ^^,  the  distance  of  the  chart  from  the 
patient  should  be  reduced.  If  the  largest  letter  is  seen 
at  eight  feet,  R  V  =  -g-fo.  If  the  top  letter  cannot  be 
read,  the  distance  at  which  fingers  can  be  correctly 
counted  is  recorded,  for  example,  R  V  =  fingers  at  one 
foot,  or,  R  V  =  fingers  at  seven  inches.  If  even  less 
vision  is  present  the  hand  is  moved  before  the  eyes;  if 
such  movements  are  appreciated  a  perception  of  haftd 
movement  is  recorded. 

If  still  less  vision  is  present,  alternately  shading  and 
exposing  the  eye  discloses  whether  there  is  a  perception 
of  light  {P.  L.)  or  not.  This  last  test  may  also  be  tried 
in  a  dark  room  by  throwing  light  upon  the  eye  by  means 
of  an  ophthalmoscopic  mirror.  Each  eye  is  tested  sepa- 
rately, one  eye  being  covered  with  a  card  or  an  opaque 
disc.  Jaeger's  test  type  is  often  used  for  testing  near 
vision. 


6o6         DISEASES   OF   THE    NERVOUS   SYSTEM. 

The  extent  of  the  visual  fields  is  best  measured  by 
means  of  the  perimeter,  the  use  of  which  is  described  in 
text-books  on  ophthalmology,  but  for  practical  purposes 
the  hand,  candle  or  blackboard  test  may  be  employed. 
Only  the  first  two  lend  themselves  for  immediate  and 
rapid  use. 

For  the  hand  test  the  patient  is  turned  with  his  back 
to  the  light,  the  examiner  facing  at  a  distance  of  about 
two  feet.  After  covering  one  eye,  the  patient  is  directed 
to  fix  constantly  the  eye  of  the  examiner  which  is  oppo- 
site. The  hand  of  the  examiner  is  then  moved  from 
various  parts  of  the  periphery  inward,  and  the  patient 
indicates  when  he  sees  the  fingers.  In  this  way  the 
examiner  compares  the  patient's  visual  fields  with  his 
own.  If  both  be  normal,  the  patient  and  examiner  must 
see  the  fingers  simultaneously.  This  method  is  simple 
and  rapid  and  is  sufficiently  accurate  for  detecting  gross 
changes  in  the  field.  If  the  patient  is  not  able  to  see 
the  hand,  a  lighted  candle  may  be  used  in  a  dark  room 
in  the  same  manner.  Contraction  defects  in  the  visual 
fields  when  on  one  side  of  the  periphery  are  indicated  as 
the  temporal,  nasal,  upper  or  lower  contraction,  or  they 
may  be  designated  as  in  the  superior,  inferior,  internal  or 
external  quadrants.  The  presence  of  peripheral  and  posi- 
tive scotoma  are  only  detected  by  the  examiner  passing 
the  hand  through  all  points  of  the  visual  fields.  The 
blind  spot  is  a  physiological  scotoma. 

An  ophthalmoscopic  examination  of  the  fundus  should 
be  made  in  all  cases  where  organic  disease  of  the  central 
nervous  system  is  suspected,  especially  where  the  symp- 
toms point  to  a  cerebral  lesion.  The  direct  method  of 
examination  is  most  generally  useful  but  should  be  sup- 
plemented when  practicable  by  the  indirect  method. 
The    technique    of    such    examination,    including    the 


EXAMINATION   OF  THE   PATIENT.  607 

method  ordinarily  used  for  measuring  the  discs  (in  case 
there  is  marked  swelling),  is  described  in  text-books  on 
ophthalmology. 

III.,  IV.  and  VI.  Motor  Oculi^  Patheiicus  and  Ab- 
ducens. — Ordinarily  the  functions  of  the  third,  fourth 
and  sixth  nerves  are  examined  together,  as  they  control 
all  the  movements  of  the  eye.  The  state  of  the  ocular 
muscles  is  disclosed  by  requiring  the  patient  to  follow 
the  finger  first  from  the  right  to  the  left  side  and  vice 
versa ^  then  up  and  down,  and  finally  by  having  the 
patient  fix  the  examiner's  index  finger  as  it  is  moved 
gradually  toward  the  nose  (convergence).  The  free 
hand  of  the  examiner  should  assist  the  patient  in  fixing 
his  head  in  the  anatomical  position  throughout  the  entire 
examination.  A  loss  of  power  in  any  muscle  is  proven 
by  {a)  limitation  of  movement,  {!))  non-compensation  of 
visual  axes,  {c)  secondary  deviation  of  the  sound  eye, 
(^)  erroneous  projection,  {e)  double  vision  and  (/)  the 
oblique  position  of  the  head. 

The  limitation  of  movement  (a)  is  always  in  the  direc- 
tion of  the  action  of  the  paralyzed  muscles;  thus  if  the 
right  external  rectus  (sixth  nerve)  is  paralyzed  there 
would  be  limitation  of  movement  in  the  right  eye  in  an 
attempted  movement  of  that  eye  toward  the  right  side. 
{J))  A  non-correspondence  of  the  visual  axes  is  noted  as 
an  internal  or  external  strabismus  in  one  or  both  eyes. 
In  the  normal  state  the  visual  axes  are  parallel  and  remain 
so  in  all  associated  movements  of  the  two  eyes. 

{c)  Secondary  deviation  is  the  most  delicate  test  of  a 
slight  paralysis  in  any  single  eye  muscle  and  is  never  pres- 
ent in  any  form  of  ordinary  squint.  When  present  this 
symptom  is  shown  if  the  sound  eye  is  prevented  from  see- 
ing the  object  by  employing  the  hand  or  a  piece  of  card- 
board as  a  screen  and  the  patient  fixes  the  object  with  the 


6o8 


DISEASES   OF   THE  NERVOUS   SYSTEM. 


affected  eye,  and  the  object  be  moved  in  the  direction  of 
the  action  of  the  paralyzed  muscle;  the  sound  eye  will 
move  still  farther  in  this  direction,  hence  the  primary 
deviation  in  the  visual  axes  is  increased  and  becomes  at 
once  noticeable.  This  is  called  "secondary  deviation." 
Its  existence  can  be  still  further  proven  by  subsequently 


DEV.'* 


FIG.    67. 

Paralysis  of  the  left  external  rectus  ;  colored  glass  over  right  eye  ;  primary  de- 
viation on  looking  towards  an  object  (o)  on  the  left ;  position  of  double  images  ; 
secondary  deviation  of  the  right  eye  when  the  screen,  s,  obstructing  the  fixation 
of  *  by  this  eye,  compels  fixation  by  the  weak  muscle.  When  the  screens  are 
moved,  the  right  eye,  in  fixing,  moves  back  to  the  position  of  the  dotted  outline 
of  the  cornea.  (In  the  diagram  of  diplopia  the  highest  white  (false)  image  should 
have  been  represented  a  little  lower  than  the  true  image.)    (Gowers.) 

covering  the  paralyzed  eye  and  requiring  the  patient  to 
fix  the  object  with  the  sound  eye,  which  then  must  move 
back  to  its  former  position. 


EXAMINATION   OF  THE   PATIENT. 


609 


In  ordinary  squint,  deviation  occurs  in  all  movements 
and  not  in  special  movement  as  in  paralytic  strabismus. 
In  ordinary  strabismus  the  deviation  is  the  same  whether 
the  patient  fixes  with  one  eye  or  the  other;  in  paralytic 
strabismus  fixation  with  the  normal  eye  evokes  the 
primary  and  that  with  the  affected  eye  secondary  devia- 
tion; the  two  are  similar  in  direction  but  opposite  in 
character.  The  primary  is  a  defect  and  the  secondary 
is  an  excess  of  movement. 

(^) Erroneous  projection. 
— The  paralyzed  eye  doe 
not  see  objects  in  their  cor- 
rect location.  The  false  pro- 
jection is  due  to  a  markedly 
increased  innervation  con- 
veyed to  the  nerve  supply- 
ing the  paralyzed  muscle  in 
an  effort  to  force  it  to  act; 
this  gives  the  patient  an  er- 
roneous idea  of  the  position 
of  the  object.  Erroneous 
projection  is  really  a  mental 
error,  an  error  of  judgment, 
and  can  be  demonstrated 
by  closing  the  patient's 
sound  eye  and  requiring 
him  to  grasp  quickly  with 
thumb  and  finger  an  object 
held  in  front.  The  grasp 
is  directed  to  the  side  of 


Diagram  to  illustrate  the  production 
of  diplopia  by  the  erroneous  projection. 
In  consequence  of  weakness  of  the  right 
external  rectus,  the  image  of  A  formed 
at  the  macula,  M,  of  the  left  eye,  falls 
within  the  macula  of  the  right  eye  at  a. 
But  the  effort  corresponds  to  that  neces- 
.,  1   .       ,  T  sary  to  bring  the  macula  to  tn  (in  the 

the      object      corresponding      broken  arO.     Hence  B,  whose  image  is 
,         .-I  11  1  at  ;;r,  seems  to  occupy  the  position  of  A, 

to     the     paralyzed     muscle.       and  the  image  formed  at /to  the  left  of 

7H  is  projected  to  the  other  side  of  A, 


1  ne  degree  Ot   lalSe  prOjeC-      and  seems  to  occupy  the  position  C,  as 

it  were  '' 
xowers.) 


.' -n    1        •  .-if  it  were  formed  at  c  to  the  left  of  w. 

tion  will  be  m  proportion    (Gc 


6lO        DISEASES   OF   THE   NERVOUS   SYSTEM. 

to  the  amount  of  paralysis;  it  is  also  increased  in  pro- 
portion as  the  paralyzed  muscle  is  required  to  act. 
Record  is  made  of  the  distance  between  the  false  and 
true  image. 

{e)  Double  vision  is  detected  by  means  of  moving  a 
lighted  candle  in  different  positions  of  the  field  of  fixa- 
tion. A  diagram  consisting  of  two  horizontal  and  ver- 
tical lines  forming  nine  spaces  held  ten  feet  from  the 
patient,  may  be  conveniently  used  for  record.  The  pa- 
tient keeps  the  head  fixed  and  merely  moves  the  eyes. 
A  red  glass  is  placed  before  one  eye  to  distinguish  its 
image.  The  candle  is  moved  about  in  different  positions 
of  Ihe  field  of  fixation  and  the  nature  of  the  diplopia  is 
noted  in  each  of  the  nine  spaces.  The  data  required 
for  record  are:  In  what  portion  of  the  field  are  there  (i) 
single  vision  and  double  vision,  (2)  whether  the  false 
image  is  on  the  same  side  as  the  weak  eye  or  crossed, 
(3)  the  relative  distance  between  the  double  images,  (4) 
whether  the  two  images  are  on  the  same  or  different 
levels,  (5)  whether  they  are  erect  or  inclined.  All  three 
symptoms  are  in  the  direction  of  the  normal  action  of  the 
paralyzed  muscle.  When  more  than  one  muscle  is  para- 
lyzed, it  is  often  difficult  to  detect  the  exact  combination. 
In  employing  diplopia  in  diagnosis  it  must  first  be  proven 
to  be  monocular  (due  to  a  dislocation  of  the  lens),  and 
that  it  ceases  on  using  one  eye  only.  It  is  easy  to  re- 
member that  when  the  prolonged  ocular  axes  are  not 
crossed  the  diplopia  is  crossed. 

(/)  There  is  a  characteristic  position  of  the  head  for 
every  variety  of  ocular  paralysis,  which  should  be  noted 
in  each  case.  The  patient  turns  the  head  toward  the 
side  of  the  paralyzed  muscle  and  in  the  direction  which 
the  muscle  would  move  the  eye  if  acting.  This  is  done 
to  diminish  or  correct  the  double  vision.     The  character 


EXAMINATION   OF   THE    PATIENT.  6ll 

and  degree  of  nystagmus  is  noted  when  present  in  testing 
for  ocular  palsy. 

V.  Trifacial  Nerve. — Inasmuch  as  disease  of  the  sen- 
sory portion  of  this  nerve  is  first  shown  by  a  loss  of  the 
sense  of  touch,  perception  and  localization  of  this  sensa- 
tion are  the  only  tests  made,  particularly  if  such  are 
negative  in  results.  For  this  purpose  two  pieces  of  cot- 
ton wool  should  be  used  and  touched  simultaneously  to 
the  same  parts  of  both  sides  of  the  patient's  face  in  the 
three  areas  of  distribution  of  this  nerve  (roughly  desig- 
nated the  forehead,  cheekbone,  and  chin)  while  the  pa- 
tient's eyes  are  closed.  He  is  then  asked  the  number  of 
times  he  was  touched,  whether  they  were  on  one  or  both 
sides  of  the  face  and  the  name  of  the  parts  upon  which 
he  was  touched.  If  the  answers  are  correct  he  should  be 
required  to  localize  these  spots  by  placing  the  finger  on 
them.  In  case  sensibility  is  shown  to  be  markedly  di- 
minished or  lost  by  this  test,  a  camel's-hair  brush  should 
be  used  to  test  the  sensibility  of  the  conjunctiva  and  the 
tongue,  while  snuff  or  ammonia  may  be  employed  to  test 
the  irritability  of  the  mucous  membrane  of  the  nose.  In 
case  touch-sensibility  is  altered,  a  complete  sensory  ex- 
amination should  follow  (for  details  of  this  method  see 
sensory  examination). 

Inasmuch  as  the  diminution  or  loss  of  the  sense  of 
taste  on  the  posterior  as  well  as  the  anterior  aspect  of  the 
tongue  is  counted  a  disease  of  the  fifth  nerve  (see  Fig. 
oo,  in  Chap.  I.),  this  sense  should  be  examined  at  this 
stage.  For  this  purpose  the  following  colorless  solid 
substances  are  used  as  they  do  not  appeal  to  any  other 
than  the  taste  sense;  sugar,  citric  acid,  salt,  and  quinine 
all  combine  the  taste  sense  of  bitter,  sweet,  sour,  and 
salt;  these  substances  are  especially  selected  as  they  do 
not  excite  the  sense  of  flavor  as  the  latter  is  appreciated 


6l2         DISEASES   OF  THE   NERVOUS   SYSTEM. 

by  the  olfactory  nerve.  Bitter  and  sweet  are  tested  for 
at  the  back,  while  sour  and  salt  are  tested  for  at  the  tip 
and  edges  of  the  tongue.  Minute  areas  are  not  to  be  tested 
as  there  are  spots  in  which  one  quality  can  be  perceived 
and  not  another.  In  the  normal  individual  there  are 
often  differences  in  the  relative  power  of  detecting  vari- 
ous substances.  The  sense  is  much  more  acute  in  the 
young  than  in  the  old.  Solids  are  used  in  preference  1o 
solutions  as  they  enable  one  to  limit  their  action  more 
easily  to  the  spots  examined.  A  little  time  should  be  al- 
lowed after  the  application  of  the  solid  for  the  powder 
to  be  dissolved  and  slight  friction  usually  facilitates  this 
latter  process.  The  tongue  should  be  kept  constantly 
protruded  during  the  test  and  a  prearranged  signal  be 
given  by  the  patient  as  soon  as  the  substance  is  tasted. 
The  voltaic  current  is  the  most  accurate  means  of  testing 
this  sense  as  it  directly  influences  the  nerve  endings.  It 
may  be  applied  by  winding  two  insulated  wires  together 
with  exposed  ends  of  a  few  millimetres  apart.  A  cur- 
rent of  one  or  two  cells  causes  a  metallic  taste  whenever 
the  function  is  intact.  More  cells  should  not  be  used 
because  pain  is  then  produced  and  obscures  the  sensa- 
tion. In  suspected  fracture  of  the  base  of  the  skull  in 
which  the  chorda  tympani  is  involved,  the  three  regions, 
the  front  of  the  tongue,  the  back  of  the  tongue,  arid  the 
palate,  should  be  especially  tested  by  this  means. 

The  resulting  loss  of  power  in  the  muscles  of  the  motor 
portion  of  the  fifth  nerve  may  be  recognized  by  placing 
the  fingers  on  the  masseter  and  temporal  muscles  of  both 
sides  and  requesting  the  patient  to  bring  the  teeth  forci- 
bly together  as  in  the  act  of  biting.  The  feebleness  or 
absence  of  contraction  on  the  affected  side  is  then  evi- 
dent. If  the  loss  in  one  muscle  is  slight  the  affected 
muscle  may  contract  a  little  slower  and  later  than  the 


EXAMINATION   OF  THE   PATIENT.  613 

Others.  Paralysis  of  the  external  pterygoids  is  detected 
(i)  by  the  inability  to  move  the  jaw  toward  the  unaffected 
side,  (2)  and  by  deviation  toward  the  paralyzed  side 
when  the  lower  jaw  is  depressed. 

In  paralysis  of  the  internal  pterygoids  the  lower  jaw 
cannot  be  thrust  forward.  In  case  there  is  only  slight 
diminution  in  power  in  any  one  of  these  muscles,  its  de- 
gree of  loss  may  be  disclosed  by  opposing  any  one  of 
these  physiological  actions.  The  downward  movement 
of  the  jaw  may  be  somewhat  limited  after  the  occurrence 
of  atrophy  and  secondary  shortening  of  the  paralyzed 
muscles  of  mastication. 

Trophic  and  spasmodic  disorders  in  the  distribution 
of  this  nerve  should  also  be  noted.  In  neuralgic  states 
either  of  functional  or  organic  basis,  the  painful  points 
and  areas  of  pain-radiation  should  be  recorded.  Uni- 
lateral furring  and  accumulation  of  food  in  the  cheek 
should  be  looked  for  in  case  there  is  a  lack  of  mastica- 
tory power  on  the  weakened  or  anaesthetic  side. 

VII.  Facial. — The  seventh  is  the  motor  nerve  of  the 
face  and  is  engaged  in  all  voluntary  and  emotional  acts. 
Its  examination  consists  in  requiring  the  patient  to 
place  each  muscle  in  action.  He  elevates  the  eyebrows, 
frowns,  closes  the  eyes  firmly,  shows  the  teeth,  whistles, 
puffs  the  cheeks,  and  smiles.  The  difference  in  volun- 
tary and  emotional  acts  should  be  noted.  In  the  state 
of  rest,  comparison  of  the  two  sides  may  be  made  for  the 
absence  of  unilateral  muscle  tone.  Secondary  overaction 
should  be  looked  for  in  facial  paralysis  after  partial  vol- 
untary power  returns.  It  is  maiked  at  rest,  but  slight 
movement  intensifies  it  while  considerable  movement  will 
disclose  the  true  naiture  of  the  muscular  defect.  An  as- 
sociated overaction  may  also  be  shown  in  the  affected 
side  in-  asking  the  patient  to  close  the  eye  in  strong  con- 


6l4        DISEASES   OF   THE   NERVOUS   SYSTEM. 

traction,  the  zygomatic!  on  the  paralyzed  side  will  then 
overact.  It  may  also  be  excited  by  reflex  action  through 
the  fifth  nerve  (Chvostek's  reflex).  The  character  and 
degree  of  spasm  if  present  should  be  examined,  first  at 
rest  and  then  during  emotional  and  voluntary  movements. 

VIII.  Acoustic. — Inasmuch  as  disturbance  of  the  func- 
tion of  the  auditory  nerve  is  much  more  frequently  due 
to  disease  of  the  ear  than  to  disease  of  the  nerve  trunk 
or  centre,  examination  must  be  undertaken  to  exclude 
the  former  in  making  a  neurological  examination:  we  are 
only  concerned  with  alterations  of  the  latter.  All  ac- 
cumulations of  impacted  wax  should  be  removed.  The 
hearing  is  most  frequently  tested  by  the  watch  held  at 
varying  distances  from  the  ear.  The  use  of  the  tuning 
fork  is  most  accurate.  The  patient  closes  the  eyes,  or, 
the  examiner's  hand  is  placed  so  that  the  patient  can- 
not see  the  progress  of  the  test.  In  case  of  deafness  by 
means  of  transmission  through  the  air,  the  watch  may  be 
heard  on  contact  with  the  external  ear.  If  air  transmis- 
sion is  not  perceived,  the  integrity  of  the  nerve  trunk 
and  centre  may  be  shown  by  bone  conduction.  This  is 
tested  by  placing  the  fork  or  watch  over  the  zygoma, 
mastoid  process,  or  at  the  root  of  the  nose.  In  case  of 
slight  deafness  in  which  the  tuning-fork  can  still  be 
heard  through  the  air,  slight  defect  in  the  meatus  or 
middle  ear  can  be  demonstrated  by  noting  that  the  tun- 
ing fork  is  heard  for  a  longer  time  through  bone  conduc- 
tion than  through  the  air.  When  vibrations  have  ceased 
to  be  appreciated  through  the  air,  the  fork  should  be 
placed  quickly  against  the  mastoid  process  and  the 
vibrations  although  diminished  in  intensity  will  still  be 
appreciated. 

Lowered  conductivity  of  the  labyrinth  is  proven  if  the 
vibrations  from  the  fork  are  not  intensified  by  closing  the 


EXAMINATION   OF   THE   PATIENT.  6l$ 

external  meatus.  Unobservant  persons,  however,  often 
fail  to  note  the  increase.  Galton's  whistle  is  a  valuable 
instrument  for  testing  the  slighter  grades  of  nerve  deaf- 
ness as  the  sound  is  high-pitched  and  of  short  duration. 
Deafness  to  all  its  sounds  is  pathological.  The  high- 
pitched  short  sound  of  the  watch  is  also  of  considerable 
value.  The  antitragus  may  be  pressed  against  the  ex- 
ternal meatus,  the  watch  may  be  held  near  the  mastoid 
or  zygoma,  but  not  against  it,  and  then  pressed  firmly 
against  the  bone.  If  the  watch  is  heard  better  in  contact 
than  when  not  in  contact,  the  function  of  the  labyrinth 
is  not  impaired.  If  it  is  not  heard  better  in  contact, 
further  observation  may  be  made  with  the  tuning-fork. 
If  the  sound  is  heard  through  the  bone  but  not  so  loudly 
as  normal,  we  cannot  infer  disease  of  the  labyrinth  or 
nerve,  because  simple  anchylosis  of  the  stapes  will  re- 
duce bone  conduction,  although  no  disease  of  the  middle 
ear  will  abolish  it.  After  fifty  years  of  age  the  watch  is 
often  not  heard  by  bone  conduction,  yet  there  may  be  no 
other  evidence  of  impaired  nerve  function.  The  loss  is 
due  to  change  in  the  labyrinth  due  to  age.  Under 
normal  conditions,  bone  deafness  is  rare  in  the  first  half 
of  life.  If  such  defect  is  unilateral,  the  rule  still  holds 
good  for  any  age.  If  Galton's  whistle  indicates  bilateral 
deafness  through  the  air  in  advanced  life,  it  is  pathologi- 
cal. Bone  conduction  indicates  the  functional  state  of 
internal  ear  and  nerve  and  eliminates  morbid  states  of 
the  conducting  media,  the  meatus  and  tympanic  cavity. 
Vibrations  pass  directly  through  the  bone  to  the  laby- 
rinth. Perversions  or  elaborations  of  simple  sounds 
into  those  of  definite  words  usually  depend  upon  changes 
most  frequently  in  some  form  of  insanity  or  epilepsy. 

Electrical  tests  to  discover  the  power  of  conductivity 
of   the  nerve   should  not  be    employed    as  they  cause 


6l6       DISEASES    OF   THE    NERVOUS    SYSTEM. 

distressing  vertigo;  their  results  are  variable  and  do  not 
always  aid  in  differential  diagnosis  between  diseases  of 
middle  ear  and  nerve.  There  are  no  tests  to  distinguish 
between  disease  of  the  labyrinth  and  nerve.  Differential 
aid  is  furnished,  however,  by  the  associated  symptoms. 
Hyperacusis  is  determined  by  the  ease  with  which  the 
high  notes  of  Galton's  whistle  are  heard.  Paralysis  of 
the  stapedius  nmscle  from  disease  of  the  facial  nerve  may 
be  shown  if  low  notes  of  the  whisile  are  heard  with  un- 
due loudness.  Pulsating  sounds  may  be  diagnosed  as 
vascular  if  they  are  found  to  be  synchronous  with  the 
pulse,  and  compression  of  the  carotids  causes  their  modi- 
fication or  cessation. 

IX.  Glosso-pharyngeal  Nerve. — Paralysis  or  weakening 
of  this  nerve  is  shown  in  requesting  the  patient  to  swal- 
low liquids  and  noting  their  regurgitation  through  the 
nose,  owing  to  imperfect  action  of  the  upper  muscles  of 
the  pharynx  innervated  by  this  nerve.  The  superior 
larynx  should  also  be  tested  for  loss  of  sensibility  as 
shown  in  the  abolition  of  the  pharyngeal  reflex  by  tick- 
ling the  throat.  There  are  no  accurate  means  of  detect- 
ing a  unilateral  impairment  of  the  nerve.  It  is  also  of 
little  clinical  importance. 

X.  Vagus  and  Accessory  Part. — Examination  of  this 
nerve  resolves  itself  for  practical  purposes  into  testing 
the  muscle  action  of  the  pharynx,  larynx,  thorax,  heart, 
and  gastro-intestinal  tract,  (i)  The  paralysis  of  pha- 
ryngeal muscles  is  usually  detected  by  the  inability  to 
swallow.  Slight  disability  in  swallowing  occurs  in  a 
unilateral  affection  of  the  nerves  if  no  physical  obstruc- 
tion to  the  act  exists.  (2)  Paralysis  of  the  larynx  may 
be  detected  by  changes  in  or  loss  of  the  voice;  an  impedi- 
ment to  the  entrance  of  air  or  an  impairment  in  the 
closure  of  the  glottis  may  be  shown  in  the  act  of  cough- 


EXAMINATION   OF   THE    PATIENT.  617 

ing.  The  defective  movements  may  also  be  directly- 
observed  by  laryngoscopy.  Com.plete  paralysis  is  shown 
by  an  absence  of  vocal  sounds  but  deep  inspiration  may 
still  cause  stridor. 

If  the  paralysis  is  complete  and  bilateral,  the  ordinary 
explosive  cough  is  changed  to  a  sudden  rush  of  air 
through  the  glottis.  One  cord  is  usually  unaffected  if 
there  is  a  low-pitched  hoarse  voice.  Slight  bilateral 
paralysis  is  demonstrated  if  the  cords  can  be  used  in 
phonation  and  cough  although  stridor  be  present  on  deep 
inspiration.  Furthermore,  ther^  will  be  no  expiratory 
stridor  and  expiration  will  be  much  shorter  than  inspira- 
tion. In  laryngeal  paralysis  the  movement  of  the  larynx 
is  much  greater  than  ever  occurs  in  tracheal  stenosis. 
These  symptoms  when  present  enable  one  to  make  posi- 
tive a  diagnosis  of  paralysis  of  the  larynx.  In  unilateral 
affection  of  the  vocal  cords  these  symptoms  may  be 
slight  or  absent  and  only  a  laryngoscopic  examination 
will  reveal  the  paralytic  state. 

Hysterical  adduction  palsy  is  always  bilateral,  and  ex- 
piration is  noiseless  although  inspiratory  stridor  may 
occur  while  speech  is  unaffected;  this  combination  of 
symptoms  differentiates  it  from  spasm  of  the  glottis. 
Phonic  paralysis  of  hysteria  is  recognized  in  adductor  ' 
paralysis,  and  in  that  the  patient  is  able  to  cough  but  is 
not  able  to  speak.  The  patient  is  also  usually  able  to 
sing  but  not  able  to  speak  in  a  whisper.  A  less  explosive 
cough  is  usually  evidence  of  organic  palsy.  Entire  loss 
of  cough  and  voice  suggests  bilateral  palsy  of  grave  im- 
port, but  loss  of  phonation  without  loss  of  speech  indi- 
cates unimportant  adduction  palsy.  Loud  inspiratory 
stridor  without  loss  of  voice  means  adduction  palsy  also. 
Loss  of  cough  without  loss  of  voice  suggests  paralysis  of 
one  cord.     The  following  scheme   will  aid  in  routine 


6l8         DISEASES   OF   THE   NERVOUS   SYSTEM. 

clinical  examining  and  recording  where  there  are  symp- 
toms of  laryngeal  paralysis. 

SYMPTOMS.  LESION. 

No    voice;    no   cough;    stridor 

only  on  deep  inspiration.         =  Total  bilateral  palsy. 
Voice  low-pitched  and  hoarse; 

no  cough;  stridor  absent  or 

slight  on  deep  breathing,  =  Total  unilateral  palsy. 
Voice   little    changed;     cough 

normal,    inspiration    difficult 

and  long  with  loud  stridor.  =  Total  abductor  palsy. 
Symptoms  inconclusive;    little 

affection  of  voice  or  cough.  =  Unilateral  abductor 
No  voice;    perfect  cough;  no  palsy. 

stridor  or  dyspnoea.  =  Adductor  palsy. 

Alterations  in  the  pulmonary,  cardiac,  and  gastric 
branches  of  the  vagus  are  to  be  diagnosticated  only  in 
the  absence  of  organic  lesions  sufficient  to  account  for 
the  symptoms  present,  organic  visceral  disease  being  ex- 
cluded. Retarded  respiration,  accelerated  or  retarded 
action  of  the  heart,  and  vomiting  are  the  more  or  less 
positive  signs  of  a  nerve  disease.  The  seat  of  disease  of 
the  vagus  is  to  be  determined  by  the  distribution  of  symp- 
toms and  their  peculiar  associated  disturbances.  Ex- 
amination discloses  much  less  frequently  a  disease  of  the 
trunk  of  the  the  nerve  than  of  the  roots  and  branches. 

XI,  Spinal  Accessory  {spinal  portion). — Paralysis  of 
the  sterno-mastoid  may  be  detected  by  the  absence  of  the 
normal  prominence  of  the  muscles,  in  movement  of 
the  head  from  side  to  side  which  may  be  measured  by  the 
observer  resisting  the  volitional  movement.  Unilateral 
defect  in  rotation  is  always  to  the  side  opposite  to  the 


EXAMINATION   OF   THE    PATIENT.  619 

paralysis.  There  will  be  no  deviation  of  the  head  at 
rest  in  simple  unilateral  paralysis  if  the  opposite  unop- 
posed muscle  does  not  produce  deviation  by  secondary 
contraction.  Complete  paralysis  and  wasting  in  the 
trapezius  may  be  demonstated  by  putting  the  muscle  at 
tension  in  straightening  the  shoulders  behind,  the  ex- 
aminer opposing  the  movement.  The  shallowness  of  the 
concave  curve  of  the  outer  side  of  the  neck  in  unilateral 
defect  is  brought  out  prominently  by  deep  respiration. 
Bilateral  palsy  of  these  two  sets  of  muscles  is  shown  in 
their  inability  to  maintain  the  head  in  the  upright  pos- 
ture. If  both  sterno-cleido  muscles  are  impaired  the 
head  tends  to  fall  back,  while  if  the  trapezii  are  both  af- 
fected the  head  readily  falls  forward  on  the  chest.  It 
falls  to  one  side  or  the  other  according  to  the  inequality 
of  the  paralysis  of  the  unilateral  two  sets  of  muscles. 
The  marked  inequality  in  the  elevation  of  the  palate  is 
best  seen  in  paralysis  when  the  patient  utters  a  long 
"ah." 

XII.  Hypoglossal. — Paralysis  of  the  tongue  is  shown, 
when  it  lies  at  rest  in  the  normal  position  in  the  mouth, 
by  the  increased  height  on  the  paralyzed  side,  due  to 
defect  in  the  posterior  fibres  of  the  hypoglossus.  -A  de- 
ficiency in  the  muscle  power  on  the  paralyzed  side 
is  shown  by  pressing  the  finger  against  the  cheek  in  which 
the  tongue  is  thrust.  On  protrusion,  however,  the  tongue 
is  deflected  toward  the  paralyzed  side,  due  to  over- 
action  of  the  unopposed  genio-glossus.  The  amount  of 
deviation  on  protruding  the  tongue  should  be  judged  by 
an  imaginary  line  drawn  vertically  between  the  upper 
two  central  incisors,  as  the  nose  often  suffers  some  de- 
flection to  the  right  or  left,  either  from  natural  asym- 
metry or  injury.  The  tongue  lies  motionless  in  complete 
bilateral  paralysis  and  cannot  be  protruded.       Slight  de- 


620 


DISEASES   OF  THE   NERVOUS  SYSTEM. 


flection  of  the  tongue  on  protrusion  may  not  be  counted 

pathological  in  the  ab- 
sence of  other  symptoms 
of  impairment  of  the 
twelfth  nerve. 

Bilateral  palsy  inter- 
feres not  only  with  artic- 
ulation but  seriously 
affects  the  processes  of 
mastication  and  deglu- 
tition. Imperfect  mast- 
ication may  be  noted  by 
the  inability  to  keep  the 
food  between  the  teeth. 
The  beginning  of  the  act 
of  swallowing  is  defective 
in  paralysis  of  the  tongue. 
Atrophy  in  the  muscles 
of  the  tongue  causes  the 
mucous  membrane  to  be 
thrown  into  irregular  lon- 
gitudinal folds,  which  is 
to  be  distinguished  from  geographical  tongue,  a  func- 
tional affection. 

Defects  of  articulation  are  shown  in  a  paralysis  of  the 
lips  (orbicularis  oris  is  probably  supplied  by  the  twelfth) 
by  requiring  the  patient  to  pronounce/,  b^  and  w,  which, 
owing  to  imperfect  closure  of  the  lips,  are  transformed 
into/  and  v.  In  palsy  of  the  tongue  the  linguals  /  and 
/  are  imperfectly  pronounced  and  tend  to  become^  and 
th.  In  palsy  of  the  palate,  the  defect  not  only  gives  an 
undue  nasal  resonance  to  the  voice  but  impairs  the  ex- 
plosive labials  /  and  b^  which  are  transformed  into  the 
continuous  labial  ;;/.     In  mild  disorders  of  the  bulbar 


FIG.  69. 

Paralysis  and  wasting  of  the  right  half 
of  the  tongue,  due  to  disease  of  the  hypo- 
glossal nerve,     (Gowers.) 


EXAMINATION   OF   THE    PATIENT.  621 

mechanism,  the  patient  may  be  asked  to  pronounce  sub- 
ordinate consonants  and  syllables;  not  only  imperfect 
enunciation  irrespective  of  their  character  will  then  be 
noted,  but  the  syllables  themselves  often  run  together 
or  are  elided.  Sometimes  consonants  are  omitted,  oi 
easier  sounds  are  substituted,  or  consonants  are  unin- 
tentionally repeated.  R  is  especially  a  source  of  exact 
trial  as  in  pronouncing  the  phrase,  "  third  riding  artillery 
brigade. "  It  is  a  classic  test  in  developing  the  paretic  type 
of  speech.  In  other  spastic  states  of  the  muscles  of  articu- 
lation a  staccato  or  scanning  speech  maybe  demonstrated. 
Examination  of  Trunk  and  Extremities. — In  conduct- 
ing the  motor  examination  of  the  trunk  and  extremities, 
the  patient  is  placed  in  the  anatomical  position  standing 
or  lying  down.  The  general  bony  framework,  its  devel- 
opment, its  departures  from  the  normal,  from  the  age, 
sex,  and  station  in  life,  and  the  presence  of  positive  de- 
formities are  noted.  The  examiner  must  carry  an  ap- 
proximate standard  of  the  normal  in  mind  if  the  lesion  is 
symmetrically  bilateral,  otherwise  a  comparison  of  the 
two  sides  may  be  made.  Allowance  must  be  made, 
however,  in  comparing  the  muscular  size  and  power  of 
the  two  sides  in  unilateral  lesions  for  the  possible  presence 
of  hypertrophy  on  the  sound  side  due  to  the  necessity  of 
increased  use  of  that  side.  The  general  state  of  muscu- 
lar development,  as  firmness,  softness,  etc.,  is  determined 
by  feeling  the  muscle  tissue  at  rest  and  in  moderate  and 
strong  contraction.  The  degree  and  completeness  of 
atrophy  or  hypertrophy  is  noted  in  the  same  manner. 
Comparative  measurements  are  not  usually  necessary  for 
practical  clinical  purposes;  the  eye  should  be  trained  so 
as  not  to  depend  upon  such  aids  for  diagnosis.  How- 
ever, when  employed  as  supplemental  data  to  an  exami- 
nation, the  following  are  of  common  use: 


622         DISEASES   OF   THE   NERVOUS   SYSTEM. 

Measurements  of  the  length  of  arm:  (from  the  acro- 
mian  process  of  the  clavicle  to  the  end  of  the  middle 
finger). 

Length  of  leg:  (from  anterior  superior  spinous  process 
of  ilium  to  the  inner  malleolus  of  the  ankle). 

Circumference  of  arm:  (at  the  middle  or  largest  part 
of  the  biceps). 

Circumference  of  forearm:  ^at  its  maximum  of  meas- 
urement just  below  the  bend  of  the  elbow). 

Circumference  of  wrist. 

Circumference  of  thigh:  {a,  at  the  gluteal  lold;  /^,  at 
the  minimum  just  above  the  patella). 

Circumference  of  leg:  (at  the  largest  part  of  calf 
muscle). 

Circumference  of  leg:  (at  its  smallest  point  just  above 
the  ankle). 

The  measurements  should  be  taken  with  a  steel  tape 
equipped  with  an  automatic  reel,  as  the  tension  of  the 
spring  can  be  relied  upon  for  drawing  the  steel  band 
uniformly  tight  in  ail  comparative  measurements.  Physi- 
ological variation  in  size  of  the  two  sides  of  the  body 
must  be  discounted  in  comparative  measurements.  Vari- 
ations of  one  half  to  three-quarter  inch  may  be  within 
normal  limits  in  the  absence  of  other  positive  data  of  a 
pathological  lesion.  Care  must  be  exercised  to  have  the 
parts  held  in  exactly  the  same  position  and  degree  of 
muscular  tension  while  comparative  measurements  are 
being  made.  All  variations  from  the  normal  position 
should  be  noted. 

Defects  in  Muscular  Power. — The  muscular  strength 
of  a  segment  of  a  limb  or  a  single  muscle  is  best  judged 
by  the  examiner  resisting  its  action.  Examination 
should  be  made  in  a  systematic  manner  from  the  proxi- 
mal to  distal  parts  of  the  extremity.      The  examiner  may 


EXAMINATION   OF   THE   PATIENT.  623 

often  experience  no  resistance,  yet  muscular  contractions 
are  sufficiently  intact  to  move  the  limbs,  particularly 
when  the  parts  are  in  certain  advantageous  positions  in 
which  muscular  action  is  greatly  assisted  by  gravity. 
The  character  and  firmness  of  the  muscular  contractions 
are  determined  by  the  examiner  placing  the  free  hand 
upon  the  laboring  parts.  The  actual  measurement  of 
muscle  power  of  the  upper  extremity  is  confined  for 
practical  purposes  to  determining  the  relative  power  of 
the  hand  grasp  by  the  instrument  known  as  the  dynamo- 
meter. The  patient  grasps  the  instrument  with  the  hand 
uppermost,  and  the  arm  is  freely  extended  from  the 
trunk,  avoiding  all  artificial  support  for  the  extremity, 
while  the  instrument  is  in  process  of  registration.  The 
relative  power  in  health  between  the  right  and  left  hand 
is  in  the  ratio  of  5  to  4  respectively.  The  rule  is  re- 
versed in  left-handed  individuals.  For  ordinary  purposes 
the  patient  grasps  the  hands  of  the  examiner.  In  ex- 
amining for  cerebral  diseases  such  as  hemiplegia,  defects 
in  segmental  movements  are  noted,  such  as  that  of  ad- 
duction, abduction,  flexion,  and  extension.  This  is 
done  because  movemeiUs  are  represented  in  the  brain 
and  not  muscles^  as  in  the  spinal  cord.  In  disease  of  the 
latter,  as  that  of  antero-poliomyelitis,  for  example,  the 
examination  of  each  muscle  or  group  of  muscles  is 
necessary. 

Actual  paralysis  is  recorded,*  as  to  (^)  range  and  (J)) 
completeness,  and  whether  such  paralysis  is  of  the  flaccid 
or  spastic  type.  If  the  latter  exists  and  cannot  be  forcibly 
overcome  by  ordinary  effort,  the  degree  of  deformity  re- 
maining is  noted  as  permanent  contracture.  If  the  para- 
lyzed muscles  have  shortened,  as  in  old  hemiplegias,  the' 
state  is  noted  as  positive  contracture,  but  if  the  unop- 
posed muscular  antagonists  have  produced  the  contrac- 


624        DISEASES  OF  THE  NERVOUS  SYSTEM. 

ture-deformity  as  in  old  spinal  palsies,  it  is  then  recorded 
as  negative  contracture.  A  condition  of  diminished 
muscle  tone  (hypotonia)  as  in  tabes  is  shown  in  the  ex- 
treme extension  of  the  joints  by  passive  means. 

Tremors  are  detected  while  the  muscle  is  at  rest  and 
in  action.  Fine  tremors  are  often  made  coarse  when 
muscles  are  placed  at  tension.  Indeed,  tremor  is  often 
detected  for  the  first  time  when  the  muscle  is  placed  at 
a  certain  degree  of  tension.  The  latter  form  of  tremor, 
however,  should  not  be  confounded  with  the  quaking, 
coarse  tremor  of  large  parts  or  a  segment,  such  as  occurs 
in  the  finger  or  hand,  called  intention  tremor,  or,  better 
still,  action  tretnor.  The  latter  is  seen  only  when  muscles 
are  at  increased  tension.  Tremors  need  to  be  noted  as 
to  their  range  (fine  or  coarse),  time  (slow  or  fast),  and 
variation  in  regularity  and  equality. 

Spasm  of  muscle  is  not  only  noted  as  tonic  or  clonic, 
but  its  degree  of  bodily  involvement,  the  excursion  or 
range  of  muscle  movement,  duration,  and  rapidity  should 
be  recorded.  It  is  essential  that  the  hand  shall  be  placed 
on  the  parts  showing  tremor  or  spasm  to  accurately  de- 
tect the  nature  and  quality  of  motor  disorders.  Simple 
inspection  often  gives  incomplete  or  deceptive  knowledge. 

The  degree  and  nature  of  inco-ordination  or  ataxia  of 
the  upper  extremities  is  best  tested  by  requiring  the  pa- 
tient to  touch  suddenly  with  the  finger  or  with  a  penci 
different  parts  of  the  body  with  the  eyes  open  and  then 
closed.  The  direction  of  movements  depends  upon  sen- 
sory elements.  It  should, however,be  remembered  that  in- 
co-ordination interfereswith  voluntarymovements  and  vice 
versa.  Standing  ataxia  or  dis-equilibration  in  the  lower 
extremities  is  noted  when  the  patient  attempts  to  stand 
with  his  eyes  closed  and  his  feet  close  together  so  as  to 
reduce  the  base  of  support.     The  patient   in  mild  de- 


EXAMINATION   OF  THE   PATIENT.  625 

grees  of  ataxy  may  also  be  made  to  stand  upon  one  foot 
alone.  A  great  many  apparently  normal  persons  show 
considerable  sway,  laterally  and  antero-posteriorly  under 
these  tests,  and  all  show  some.  Neurasthenics  are  apt 
to  show  wide  variations.  If  the  patient  falls  or  tends 
to  fall  under  these  tests,  it  is  called  static  ataxy  or  Rom- 
berg's symptom.  Ataxy  in  the  gait  is  brought  on  by  the 
patient  walking  a  chalk  line  or  a  crack  in  the  floor  by 
what  is  known  as  "  heel  and-toe  gait."  At  the  end  of 
the  line  or  crack  the  patient  should  be  required  to  turn 
sharply  at  command  and  retrace  his  steps.  Slight  degree 
of  defective  equilibration  is  often  shown  only  in  the 
act  of  turning.  Inco-ordination  or  ataxy  is  usually  in- 
creased if  the  patient  walk  with  the  eyes  closed. 

In  examining  the  muscles  of  the  trunk,  especially  when 
compression  paraplegia  occurs  at  the  lumbar  segment, 
the  rising  of  the  umbilicus  should  be  noted.  This  is  de- 
termined by  the  examiner  holding  the  finger  at  the  level 
of  the  umbilicus  and  requesting  the  patient  to  sit  up. 
The  umbilicus  will  be  seen  to  rise  from  i  to  3  inches  ac- 
cording to  the  degree  of  paralysis  of  the  rectus  abdominis. 

The  spine  should  be  examined  for  deformity  and  ten- 
derness. The  latter  is  tested  by  laying  the  flat  hand  or 
fist  over  the  vertebra  in  which  disease  is  suspected,  then 
strike  this  forcibly  with  the  other  fist. 

Reflexes. — For  convenience  and  thoroughness  of  ex- 
amination the  following  superficial  and  deep  reflexes  are 
examined  in  the  order  given. 

SUPERFICIAL.  DEEP. 

Conjunctival  and  corneal.  Pupillary. 

Cilio-spinal.  Trigemino-facial. 

Scapular.  Jaw  jerk.   . 

Abdominal  and  epigastric.  Pectoral. 
40 


626        DISEASES   OF  THE  NERVOUS  SYSTEM. 

Cremasteric.  Elbow — biceps  and  tri- 

ceps. 
Gluteal.  Wrist  —  supinator      and 

ulnar. 
Knee-jerks. 
Achilles. 
Front  tap. 
Babinski. 

The  conjunctival  and  corneal  reflexes  are  tested  by- 
contact  of  a  twisted  bit  of  cotton-wool.  The  eyelashes 
should  not  be  touched  in  making  the  examination. 

The  cilio-spinal  is  obtained-by  pinching  the  skin  at  the 
nape  of  the  neck  at  which  the  pupils  should  dilate.  The 
scapular  is  shown  by  stroking  the  skin  between  the 
shoulder-blades;  the  response  is  noted  by  the  inner-lower 
angles  of  the  shoulder  approximating  the  spinal  column. 
A  quick  sharp  stroke  of  the  finger-nail  or  the  end  of  a 
match  along  the  free  border  of  the  ribs  brings  out  the 
abdominal  reflex.  The  epigastric  reflex  is  demonstrated 
by  stroking  the  hypogastrium.  The  same  sort  of  stroke 
on  the  inner  side  of  the  thigh  in  man  shows  a  sharp  re- 
traction of  the  testicle  of  the  same  side.  The  gluteal 
reflex  is  produced  by  irritating  the  skin  just  above 
the  gluteal  fold.  By  stroking  the  sole  of  the  foot 
it  is  retracted,  which  demonstrates  the  plantar 
reflex. 

Inasmuch  as  the  deep  reflexes  are  of  greater  clinical 
significance,  every  precaution  should  be  taken  to  exclude 
error  in  making  the  necessary  tests.  In  ordinary  tests  the 
pupillary  reflex  is  obtained  by  causing  the  patient  to  face 
a  window  in  such  a  manner  that  there  shall  be  an  equal 
lighting  of  both  eyes,  while  the  examiner  alternately  and 
conjointly  exposes  and  screens  the  eyes  with  his  hands. 


EXAMINATION   OF   THE   PATIENT.  62^ 

If  the  pupils  dilate  and  contract  in  dark  and  light  re- 
spectively, the  pupil  is  said  to  show  light  action^  if  not, 
light  inaction.  The  test  for  accommodation  is  made  by 
asking  the  patient  to  fix  first  some  near  and  then  some 
far  object  while  the  light  upon  the  two  objects  remains 
the  same;  if  the  pupils  respond,  the  test  is  indicated  as 
far.,  and  near  action. 

The  preservation  of  far  and  near  action  while  there 
is  light  inaction  is  the  condition  known  as  the  Argyll- 
Robertson  pupil.  In  case  there  is  doubt  whether  ac- 
commodation to  distance  may  cause  the  slight  change 
in  the  pupils  during  the  light-action  test,  the  patient 
should  be  required  to  fix  definitely  upon  some  objective 
point,  the  examiner's  nose,  for  example,  in  a  dimly 
lighted  room,  and  a  candle  or  match  may  then  be 
brought  from  behind  the  patient's  head  to  a  position  in 
front  of  the  face  so  the  rays  of  light  may  fall  upon  the 
pupil.  In  this  way  one  may  definitely  exclude  the  pos- 
sibility of  far  and  near  action  confusing  the  light  test. 
The  reflected  light  from  a  mirror  may  be  also  used  in- 
stead of  a  match  or  candle;  the  pupillary  accommodation 
to  distance  can  thus  be  absolutely  excluded. 

The  jaw  jerk  is  shown  by  tapping  the  finger  which  de- 
presses the  lower  jaw  during  slight  muscular  tension. 

The  biceps  jerk  is  obtained  by  placing  the  forearm  at 
a  slight  angle  with  the  arm  and  tapping  the  finger  laid 
on  the  biceps  tendon.  The  triceps  jerk  is  obtained  by 
a  direct  tap  on  the  muscle  tendon  above  the  olecranon. 
The  arm  is  partly  supported  by  the  examiner,  the  fore- 
arm being  allowed  to  hang  loosely.  The  supinator  jerk 
is  obtained  by  a  direct  tap  on  the  muscle  midway  be- 
tween the  elbow  and  wrist  while  the  forearm  is  moderately 
flexed.  The  ulnar  jerk  may  be  shown  by  striking  the 
tendon  of  the  extensor  carpi  ulnaris,  or  the  ulnar  bone 


628 


DISEASES   OF  THE   NERVOUS   SYSTEM. 


itself,  along   the   shaft  where  the   latter  becomes  sub- 
cutaneous 

The  presence  or  absence  of  the  knee-jerk,  the  most 
important  muscle  jerk,  is  determined  by  having  the  knee 
so  flexed  that  the  quadriceps  femoris  is  gently  extended. 
If  then  the  patellar  tendon  is  struck,  the  quadriceps 
contracts  and  the  lower  leg  is  jerked  forward  if  free  to 
move.    (Fig.  70.)    The  blow  is  given  over  the  space  above 


FIG.  70. 

The  knee-jerk.     The  dotted  line  indicates  the  movement  which  follows  the 
blow  on  the  patellar  tendon.     (Gowers.) 

the  tibia  where  the  tendon  can  yield  if  there  is  a  sudden 
increase  in  the  tension  of  the  muscle.  The  most  con- 
venient position  is  with  the  knee  to  be  tested  flexed 
nearly  but  not  quite  at  a  right  angle,  by  being  placed 
over  the  other  knee  as  the  person  sits.  If  the  leg  to 
be  tested  is  stout,  its  tension  in  this  position  may  be 
too  great  to  permit  of  any  movement.  In  such  a  case 
the  examiner  may  place  his  arm  beneath  the  patient's 


EXAMINATION   OF  THE   PATIENT. 


629 


thigh  just  above  the  knee  and  rest  his  hand  on  the 
patient's  other  knee.  Muscular  relaxation  is  sometimes 
more  readily  obtained  when  the  leg  hangs  vertically  or 
the  foot  rests  on  the  floor,  and  the  contraction  be  appre- 
ciated by  the  hand  placed 
directly  on  the  muscle;  the 
effect  of  the  recoil  and  of  the 
muscular  contraction  must 
then  be  carefully  distin- 
guished. If  the  bent  fingers 
of  the  hand  are  hooked  to- 
gether and  the  eyes  closed, 
the  movement  is  increased 
in  degree — termed  reinforce- 
ment. It  is  essential  that 
the  flexors  also  should  be 
free  from  voluntary  contrac- 
tion. This  contraction  can 
be  ascertained  by  feeling  the 
hamstring  tendons,  and  pres- 
sure on  these  by  the  fingers 
often  helps  to  secure  relax- 
ation. The  blow  may  be 
given  by  the  side  of  the  hand, 

a  percussion  hammer  specially  devised  for  this  purpose 
or  a  continental  stethoscope  with  an  india-rubber  edge 
to  the  ear-piece.  When  the  jerk  is  doubtful  the  skin 
should  be  bared. 

The  same  contraction  may  also  be  obtained  by  other 
modes  of  suddenly  increasing  the  muscle  tension,  espe- 
cially when  the  excitability  is  abnormal  in  degree.  A 
blow  on  the  tibia  may  be  effective.  While  the  patient  is 
in  the  recumbent  position  with  the  muscles  relaxed  the 
patella  may  be  displaced  downward  by  a  finger  placed 


FIG.  71. 

The  knee-jerk.  Method  of  obtain- 
ing it  when  it  is  not  readily  produced 
in  the  ordinary  way.    (Gowers.) 


630 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


across  the  upper  edge ;  tap  the  finger  so  as  to  suddenly 
displace  the  finger  in  the  direction  of  tension;  this  excites 
the  contraction  of  the  muscles  even  where  there  is  but 
slightly  increased  excitability.  If  the  muscle  tension  be 
maintained  after  the  tap  and  there  be  great  excitability 
of  the  muscle  clonus,  repeated  rhythmic  jerks  may  per- 
sist while  the  tension  lasts.  Similar  contraction  may  be 
induced  in  other  muscles  susceptible  of  the  same  treat- 
ment. The  Achilles  jerk  is  brought  out  by  gently  press- 
ing the  foot  up,  thus  increasing  the  tension  of  the  calf 
muscles;  the  tendon  is  then  tapped,  the  muscle  con- 
tracts and  causes  slight  extensor  movement  of  the  foot. 


FIG.  72. 

Method  of  eliciting  the  foot-clonus.     (Gowers.) 

(Fig.  72.)  A  tap  on  the  side  of  the  tendon  is  equally 
effective,  but  if  the  tendon  be  so  firmly  supported  as  not 
to  permit  the  foot  to  yield,  the  hand  must  be  placed  on 
the  calf  muscles  to  appreciate  the  contraction.  The 
cause  of  the  suddenly  increased  muscle  tension  is  the 
stimulation  and  not  the  blow  on  the  tendon   itself.     If 


EXAMINATION   OF  THE   PATIENT.  63 1 

the  excitability  of  the  calf  muscles  be  excessive  the  test 
for  the  Achilles  jerk  may  excite  an  ankle  clonus. 

The  front  tap  is  best  tested  by  smartly  tapping  the 
tibialis  anticus  with  the  hammer  or  stethoscope  while  the 
foot  is  flexed  dorsally  by  the  observer.  The  ankle  should 
rest  on  the  examiner's  knee  or  on  the  edge  of  a  stool 
placed  slightly  lower  than  the  chair  upon  which  the  pa- 
tient sits,  or  with  the  leg  extended  if  the  patient  is  in 
bed.     The  reflex  consists  in  plantar  flexion  of  the  foot. 

In  examining  for  Babinski's  toe-phenomenon  all  pos- 
sible agents  complicating  the  response  must  be  excluded; 
the  foot  should  be  warm,  the  leg  partly  flexed  to  aid 
muscular  relaxation  of  the  parts  and  to  avoid  the  occur- 
rence of  voluntary  movements  while  the  test  is  being 
made.  The  outer  sole  of  the  foot  is  stroked  more  or  less 
slowly  by  the  thumb-nail  or  a  piece  of  match.  If  this 
pathological  sign  be  absent,  the  plantar  flexion  of  the  big 
toe  is  observed,  but  if  present,  the  toe  is  dorsally  flexed, 
or  the  flexor  longus  proprius  tendon  is  seen  to  flick  up 
notwithstanding  the  muscle  action  is  not  sufficient  to 
actually  move  the  big  toe.  The  movements  of  the  other 
toes  should  be  disregarded.  They  may  or  may  not  co- 
incide in  the  big  toe  movements. 

Electrical  Examination. — In  making  the  electrical  ex- 
amination the  sponges  should  be  kept  wet  by  frequent 
dipping  in  a  weak  solution  of  common  table  salt  or  bi- 
carbonate of  soda.  When  examination  for  reaction  of 
degeneration  by  means  of  polar  changes  is  made,  as  a 
matter  of  convenience,  one  pole  (indifferent  electrode) 
should  consist  of  a  large  flat  sponge  pad  applied  over  the 
sternum,  at  the  sacrum,  or  nape  of  the  neck.  The  patient 
must  fully  relax  the  muscles  to  be  tested.  The  exciting 
electrode  should  have  a  small  surface  to  concentrate  the 
current.     The  amount  of  electricity  passing  should  be 


632         DISEASES   OF  THE  NERVOUS   SYSTEM. 

gauged  by  a  galvanometer,  as  in  a  reversal  of  the  poles 
frequently  less  current  passes  during  the  first  two  or 
three  applications  of  the  isolated  shocks.  A  decision 
that  a  polar  change  exists  should  be  inferred  only  when 
there  is  an  equal  amperage  to  both  positive  and  negative 
current  at  the  point  of  test.  In  the  milder  stages  of 
nerve  degeneration  the  sloivness  of  muscular  contraction  is 
noted  as  a  slight  sign  of  R.  D.  in  the  absence  of  positive 
polar  change.  In  children  and  in  sensitive  individuals 
it  is  preferable  to  use  the  isolated  induced  shock  as  it  is 
less  painful.  Before  actually  applying  the  current  the 
examiner  should  first  receive  the  current  upon  his  own 
person  for  the  sake  of  safety  to  the  patient  and  to  mini- 
mize the  patient's  sense  of  fear  of  the  proposed  test. 
Faradization  should  be  first  tried  and  if  the  reaction  is 
normal  galvanism  is  unnecessary.  In  case  there  is  a 
diminished  or  lost  response  to  faradism  (although  not 
necessary  for  diagnosis),  galvanism  may  be  employed  for 
the  purpose  of  prognosis.  The  minimum  of  galvanic 
current  to  which  an  electric  response  may  be  obtained 
should  always  be  employed.  Many  times  when  there  is 
a  slight  but  equal  diminution  of  responses  to  both  poles, 
the  degree  of  departure  from  the  normal  can  be  deter- 
mined by  comparing  the  same  parts  of  the  sound  side 
with  those  diseased,  or  in  case  of  a  bilateral  lesion  an 
analogous  part  in  a  sound  extremity  may  be  used  for 
comparison.  The  designation  "lost"  as  applied  to  an 
absent  response  means  a  negative  test  to  that  current 
which  can  be  borne  by  the  patient  without  great  pain. 
Even  under  such  circumstances  a  response  might  still  be 
gained  under  anaesthesia,  but  for  practical  purposes  such 
a  procedure  is  never  necessary.  Fig.  73  and  Fig.  74 
show  the  motor  points  of  the  inner  and  outer  side  of 
upper   extremity,   while   Fig.    75    and    Fig.    76   are   the 


Triceps  (long  head) 

Triceps  (inner  head) 
Ulnar  n.  ■< 


Flex,  carpi  ulnar. 
Flex.  dig.  profund. 

Flex.  dig.  snh.  (II  &  III) 

Flex,  digit,  sub.  (I&IV) 
Ulnar  n. 

Palm,  brev. 

Abd.  minim,  digit. 

Flex.  min.  dig. 

Oppon.  min.  dig. 

Lombricales 


Deltoid 
(ant.  half) 


Mus.-cut. ». 

Biceps 

Brach.  ant. 

1 

^  Median  n-. 

Supinator  long. 
Pronator  teres 
Flexor  carpi  radialis 

Flex,  digitor   sublim. 

•  Flex.  long,  pollicis 

Median  n. 

Adductor  pollicis 
Opponens  pollicis 

Flex.  brev.  pollicis 

Adductor  pollicis 


FIG.    73. 

Motor  points  for  the  arm,  inner  side  (from  Erb).     The  points  at  which  the 
muscles  and  nerves  can  most  effectively  be  stimulated. 


633 


634 


DISEASES   OF   THE   NERVOUS   SYSTEM. 


Deltoid 
(posterior  half) 


Mu»c.-spiral  n 
Brachialis  ant. 

Supinator  longus 
Extensor  radial,  long. 
Extensor  radial,  brev. 


Extensor  d 
Extensor  indicis 

Ext.  OS.  met.  pol. 
Extensor  pr.  intern,  pol. 


Dorsal  interossei  J 
(I  and  II)        1 


Triceps  (long  head) 


V  Triceps  (outer  head) 


Extensor  carpi  uln. 
Supinat.  brev. 

Extens.  minim,  digiti 
Extensor  indicis 

y  Extens.  long.  poll. 


Abduct,  minim,  digiti 
•"[Dorsal  interossei 
/    (III  and  IV) 


FIG.   74. 
Motor  points  for  the  arm,  outer  side  (Erb.) 


EXAMINATION   OF  THE   PATIENT.        635 

Standard  guides  for  the  motor  points  of  the  leg,  inner 
and  outer  side. 

The  sensitiveness  of  the  skin  differs  in  different  indi- 


Tibialis  anticus 
Extensor  digit, 


Peroneus  brevis 


Extensor  long.  poll. 


Dorsal  interossei 


Ext.  poplU.  a. 


Gastrocnera.  (outer  head) 
Peroneus  longus 


V  Soleus 


Flexor  long,  pollicis 


Eztensor  brev.  digit. 


Abductor  minim,  digit. 


FIG.   75. 
Motor  points  of  leg,  outer  side  (Erb). 

viduals  and  in  different  parts.  The  resistance  of  the 
skin  also  varies;  the  greater  it  is,  the  stronger  must  be  tlie 
current  used  to  secure  the  action  on  the  nerves  below. 


636        DISEASES  OF  THE  NERVOUS  SYSTEM. 

Hence  the  importance  of  ascertaining  what  current  is 
actually  passing  by  use  of  the  galvanometer.     It  may  be 


Sciatic  n.  " 


Biceps  (long  head) 
Biceps  (short  head) 


"Ext.  poplif.  n. 
Qastrocnem.  (ext.  head) 

Soleus 
Plexor  long.  poll. 


i-  Gluteus  maximus 


Adductor  magnus 

• r~~Setnitendinosus 

Semimembranosus 


Int.  popUt.  n, 

Gastrocnem.  (int.  head) 
Soleus 

Flexor  digit,  comm. 
Tibial  n. 


FIG.    76. 
Motor  points,  back  of  thigh  and  leg  (Erb). 


used  once  to  gain  information  as  to  the  significance  of 


EXAMINATION   OF  THE   PATIENT.  637 

the  number  of  cells  that  constitute  the  evidence  of  the 
difference  between  the  two  sides,  when  the  sensitiveness 
to  the  pain  which  is  caused  prevents  the  use  of  this  in- 
strument in  all  measurements.  In  complete  reaction  of 
degeneration  the  muscles  also  should  be  percussed  to  see 
if  mechanical  excitability  is  also  present  as  shown  by  the 
slow  muscular  contraction  in  the  part  of  the  muscle 
struck. 

Sensory  Examination. 

Sensibility  to  Touch. — The  structures  that  subserve 
tactile  sensibility  are  stimulated  chiefly  by  change  in 
contact.  Prolonged  contact  uniform  in  degree  and 
place  is  perceived  but  little  and  only  by  close  attention. 
It  is  change  that  excites  an  impulse.  The  commence- 
ment of  contact  is  more  effective  than  its  cessation. 
Rapidity  of  change  determines  the  result  of  the  test. 
A  firm  pressure  is  scarcely  noticed  if  it  be  gradual  in  its 
application,  while  a  sudden  touch  is  observed  however 
light.  In  testing  tactile  sensibility,  the  instrument  em- 
ployed must  not  arouse  any  other  sense  as  heat  or  cold, 
such  as  the  finger  may  do;  cotton-wool  should  therefore 
be  employed.  The  eyes  should  be  closed,  as  the  patient 
is  apt  to  fancy  that  a  light  touch  is  felt  when  none  is 
made.  The  patient  should  occasionally  be  asked  if  he 
can  feel  when  no  contact  is  made.  One  should  touch 
irregularly  in  point  of  time  and  degree,  and  then  not  at 
all,  and  ask  after  the  latter  procedure  if  something  is  still 
felt  as  before.  It  is  nearly  as  easy,  however,  to  make 
the  test  too  fine  as  too  gross.  If  the  skin  be  thick,  sensi- 
bility of  the  skin  is  normally  low,  and  light  touch  is  often 
unappreciated  in  the  healthy  under  such  conditions. 
The  test  employed  may  be  tried  on  the  examiner  himself, 
which  affords  a  normal  standard  always  at  hand.  The  term 


638         DISEASES   OF   THE   NERVOUS   SYSTEM. 

'*  sensibility  to  touch"  should  be  used  instead  of  ''anaes- 
thesia,"  as  the  latter  is  often  inaccurately  used.  The 
patient  should  not  only  be  asked  if  he  feels  a  touch,  but 
should  be  required  to  name  the  part  touched  and  be  able 
to  localize  it  with  the  finger.  The  part  touched  should 
be  constantly  varied,  so  the  patient  may  not  become 
schooled  to  the  examination.  The  acuteness  of  touch 
sensibility  is  subject  to  a  certain  degree  of  measurement, 
as  the  distance  apart  at  which  two  points  are  discon- 
nected is  nearly  the  same  in  different  individuals  in  the 
same  part  of  the  body,  although  it  varies  much  in  differ- 
ent parts  of  the  same  person.  The  approximate  normal 
distance  being  known,  the  increased  distance  at  which 
two  points  have  to  be  placed  for  their  discrimination  is  a 
measure  of  the  degree  of  defect.  The  points  should  be 
a  little  dulled  so  as  not  to  cause  pain.  Common  com- 
passes may  be  employed,  but  the  most  convenient  aesthesi- 
ometer  is  Sieveking's  in-  which  the  points  are  attached 
to  a  graduated  bar.     The  principal  points  are: 

Tip  of  tongue 1.5  min. 

Finger-tips 2  to  3  min. 

Lips 4  to  5     " 

Tip  of  nose 6  min. 

Cheeks  and  back  of  fingers 12 

Forehead ' 22 

Neck 34 

Forearm,  lower  leg,  and  back  of  foot. 40 

Chest 45 

Back 60 

Upper  arm  and  thigh 75 

The  distance  is  smallest  at  the  tip  of  the  tongue— that  is, 
the  sensitiveness  is  greatest.     The  most  important  aver- 


EXAMINATION   OF   THE   PATIENT.  639 

age  distance  is  the  normal  at  which  two  points  can  be 
recognized. 

Slight  variations  exist  in  different  individuals,  and  a 
deviation  from  the  normal  that  is  uniform  in  degree 
throughout  the  body  is  probably  physiological.  The  skin 
must  be  touched  at  the  same  time  and  with  equal  degree 
of  pressure  by  both  points.  The  examination  requires 
time  and  patience.  Increased  power  of  discrimination 
on  the  part  of  the  patient  is  acquired  by  practice.  Con- 
clusive results  are  rarely  obtained  unless  there  is  a  degree 
of  defect  that  causes  absolute  loss;  the  test  is  therefore 
of  much  less  practical  value  than  was  once  thought. 

Sensibility  io  pain  is  subserved  by  nerves  of  common 
sensibility;  it  is  usually  tested  by  a  blunt  pin-prick.  A 
finer  instrument  such  as  a  needle,  should  not  be  used;  it 
may  not  only  penetrate  the  skin,  but  in  less  sensitive 
parts  where  nerve  endings  are  not  close  together  a  fine 
point  may  be  unfelt  although  readily  near  by.  The  wire 
terminals  of  a  faradic  battery  need  to  be  applied  with 
great  care  and  the  current  carefully  graduated  if  gain  in 
exactness  is  to  be  obtained  over  that  by  the  use  of  a  pin- 
prick. Touch  may  produce  pain  if  the  common  sen- 
sibility is  greatly  increased.  Both  tactile  and  painful 
impressions  may  produce  subjective  sensations  distinctly 
abnormal,  such  as  thrilling,  tingling,  etc. 

When  a  prick  is  only  perceived  as  touch,  pain  may  not 
be  lost  but  only  delayed,  as  the  patient  only  names  the 
sensation  first  felt.  The  patient  should  be  asked  to 
name  the  sensations  the  instant  they  are  perceived  and 
whether  any  new  sensation  is  perceived  after  when  sense 
of  touch  is  intact.  The  test  to  pain  must  be  kept  uni- 
form, gauged  in  amount  by  exposing  only  a  small  part  of 
the  pin-point  between  the  fingers.  Sensibility  to  pain  is 
often  diminished  but  not  lost.     Patients  often  mistake 


640        DISEASES   OF  THE  NERVOUS  SYSTEM. 

the  degree  of  pain  they  should  recognize  and  often  vary 
this  idea  during  the  examination;  to  avoid  these  two 
errors,  frequent  comparisons  to  some  approximate  stand- 
ard of  sensibility  in  another  part  of  the  body  should  be 
made.  To  these  errors  must  often  be  attributed  the 
variation  and  unreliability  of  many  examinations. 

Temperature  Sense. — While  sensibility  to  pain  may 
vary  although  touch  is  intact,  temperature  is  usually 
affected  with  sensibility  to  pain,  but  often  not  in  the 
same  degree,  and  one  may  be  impaired,  as  in  syringo- 
myelia, without  the  other.  Slight  losses  of  temperature 
sense  may  not  be  detected,  or  there  may  be  an  absolute 
loss  to  both  heat  and  cold  as  such. 

While  considerable  degrees  of  difference  are  recog- 
nized correctly,  a  quality  of  difference  is  perceived  analo- 
gous to  that  noted  in  the  perception  of  difference  of 
pressure.  Hot  objects  may  feel  cold,  and  vice  versa. 
Ordinary  temperature  may  produce  pain,  or  heat  may 
be  less  readily  perceived  than  normal.  In  cases  show- 
ing an  increased  lapse  in  time  between  application  of  pin- 
prick, a  similar  delay  in  temperature  test  is  so  shown. 
In  health,  temperature  sense  is  less  quickly  produced 
than  that  of  pain,  because  time  is  required  to  raise  the 
temperature  of  the  skin  sufficiently  to  enable  the  heat  to 
stimulate  its  nerves. 

For  rough  examination  hot  and  cold  spoons  may  be 
employed,  or  a  hinged  tongue  depressor,  one  blade  of 
which  may  be  heated ;  better  still  two  similar  test-tubes 
containing  hot  and  cold  water  may  be  used.  Both  heat 
and  cold  must  be  sufficient  in  degree  to  be  unquestion- 
able, so  that  the  patient's  doubt  may  be  definitely  re- 
corded as  pathological  and  not  due  to  the  uncertainty 
of  lukewarmness  of  the  testing  object.  For  ascertaining 
the  power  of  differential  discrimination,  large  test-tubes 


FIG.  77. 


641 


-Sac.2 


tiu.  78. 


643 


EXAMINATION   OF   THE   PATIENT.  643 

may  be  employed  containing  water  of  known  temperature, 
indicated  by  a  thermometer  in  each.  The  accuracy  of 
test  of  the  pain  sense  may  be  verified  in  a  rough  way  by 
heating  the  hot-water  test-tube  to  that  point  at  which 
pain  is  produced.  Sensibility  to  heat  and  cold  should 
be  tested  separately  at  some  time  during  the  examination 
as  the  two  sensations  are  subserved  by  different  nerves. 
Some  minute  points  appreciate  only  heat  while  others  in 
a  like  manner  appreciate  cold  only.  Finally  the  two 
sensations  maybe  affected  in  different  degrees.  Fig.  77 
and  Fig.  78  show  approximately  the  sensory  skin  areas  of 
the  different  spinal  cord  segments  devised  by  Head. 

Muscular  sense  includes  more  than  one  sensation;  it 
embraces  muscle  pain  sense.  The  afferent  impulses  origi- 
nate from  the  muscle  spindle  which  is  excited  by  pressure 
and  traction.  The  latter  is  tested  by  gripping  the  belly 
of  a  muscle  and  comparing  the  uncomfortable  or  painful 
sensation  thus  produced  with  a  similar  test  in  a  sound 
muscle,  or  in  general  employing  an  imaginary  standard 
of  test.  Postural  sense  is  ascertained  either  at  rest 
or  in  action  from  cutaneous,  joint,  or  muscle  structure, 
but  probable  most  from  the  knowledge  of  muscle  tone 
or  tension.  Our  recognition  of  resistance  to  contrac- 
tion affords  one  of  the  most  delicate  tests  for  muscu- 
lar sensibility.  It  is  ascertained  by  detecting  difference 
of  weight — that  is,  variation  in  the  resistance  to  con- 
traction. The  patient's  eyes  should  be  closed  during 
the  trial.  Objects  of  uniform  size,  such  as  leather  balls 
the  size  of  golf  balls  which  contain  various  weights  from 
two  drachms  to  two  pounds,  may  be  selected  for  this 
purpose.  Cutaneous  sensibility  may  be  reduced  to  a 
minimum  by  placing  the  weight  in  a  bag  suspended  by  a 
string  on  the  parts  to  be  tested;  or  increase  the  area  of 
suspension  and  thus  diffuse  it  in  diminished  degree,  or 


644         DISEASES   OF   THE   NERVOUS   SYSTEM. 

increase  the  weight  and  therefore  the  pressure  in  both 
area  and  degree  so  that  the  addition  to  be  discovered 
shall  bear  only  a  small  proportion  to  the  total  stimula- 
tion. The  discrimination  of  weights  by  muscular  sensi- 
bility is  greater  than  by  the  skin;  a  difference  of  4*0  of 
the  total  weight  may  be  appreciated  by  the  former.  The 
electrical  test  of  the  sensibility  of  the  skin  is  not  practi- 
cal. The  sensibility  of  muscle  to  the  electric  current 
can  only  be  ascertained  by  eliminating  that  of  the  skin 
by  cocaine  anaesthesia. 

A  rough  and  practical  but  rather  inaccurate  test  for 
muscular  sensibility  is  the  power  of  recognizing  passive 
posture.  If  cutaneous  sensibility  is  normal  the  parts 
handled  must  be  grasped  firmly  and  pressed  on  both  sides 
so  that  the  direction  of  pressure  may  not  suggest  the  pos- 
ture. The  patient  may  be  asked  to  place  the  limb  of  the 
other  side  in  the  same  posture  or  indicate  the  direction  of 
movement  with  the  finger.  Several  examinations  should 
be  made  to  determine  the  chance  of  accidental  error. 
Data  of  disorders  of  touch,  pain,  and  temperature  sensi- 
bility should  be  charted  on  outline  figures  made  espe- 
cially for  this  purpose.  Written  descriptions  of  such  data 
are  too  confusing  and  obscure  for  rapid  reference  in  a 
clinical  study  of  the  case.  The  stereognostic  sense  is 
best  tested  by  requiring  the  patient  to  recognize  with 
closed  eyes  the  size,  weight,  and  form  of  various  familiar 
objects  at  hand  such  as  keys,  coins,  etc. 

Disorders  of  General  Functions  and  Visceral  Examination. 

Aphasia. — If  the  speech  defect  is  not  an  articulatory 
one  it  is  called  aphasia  and  it  is  necessary  to  apply  cer- 
tain tests  for  the  determination  of  the  exact  difficulty. 
In  routine  examination  one  tests  in  turn  the  integrity  of 


EXAMINATION   OF  THE   PATIENT.  645 

the  motor  memory,  visual  memory,  and  auditory  memory. 
To  appreciate  the  condition  of  the  motor  speech  centre 
and  its  as.sociation  tracts,  the  examiner  must  note  the 
patient's  ability  to  speak  voluntarily  and  his  ability  to 
repeat  words  spoken  by  the  observer.  To  test  visual 
speech  one  must  test  the  patient's  capacity  to  understand 
written  or  printed  words;  his  ability  to  write  spontane- 
ously, his  ability  to  write  common  things  he  sees,  such 
as  knife,  button,  etc.,  which  he  hears,  or  which  he 
touches;  his  ability  to  copy  writing;  his  ability  to  under- 
stand written  directions  as  shown  by  his  ability  to  exe- 
cute them.  To  test  the  integrity  of  the  auditory  speech 
and  its  association  the  following  are  to  be  noted:  the 
power  of  the  patient  to  recall  names  of  familiar  objects 
seen,  heard,  touched,  etc. ;  ability  to  understand  ordi- 
nary speech,  and  his  ability  to  recognize  musical  airs 
(whistling  Yankee  Doodle^  for  example). 

Vaso-motor  and  Trophic  Disorders  should  be  noted  as 
expressed  in  ulcers,  nutrition  of  skin,  hair,  nails,  and 
changes  in  color  and  heat  of  the  skin  in  different  parts 
of  the  body.  Aside  from  a  thorough  visceral  examina- 
tion, such  as  is  made  in  internal  medicine,  of  the  blood, 
urine,  temperature,  pulse,  etc.,  the  condition  of  the 
sphincters  is  to  be  especially  noted  in  spinal  affections. 
Incontinence  of  the  bladder  occurs  under  three  different 
conditions,  (^)  in  general  lowered  cerebral  function,  as 
in  tumor  cases  where  through  neglect  of  the  personal 
toilet  a  retention  and  final  overflow  is  permitted,  (/') 
paralytic  incontinence  through  loss  of  sphincter  control, 
as  in  spinal  paralysis,  and  (<r)  incontinence  due  to  mental 
defect,  as  seen  in  idiocy. 


a 
•1-1 

u 

o 
o 

o  > 

O  -M 
^  Oh 
1^      ^ 

B  o 

<u  ^ 
03  cj 
-t-J      CD 


o 
a 


CO 

CO 


0) 

<:^ 

w 

(D 

O 

c3 
o 

a 

c^ 

cu 

bx) 

g 

-t-s 

j:: 

-Si 

't-i 

.  i-H 

o 

w 
O 

^ 

a 

o 

o 

a 

X 

a; 

o 

On 

tuD 

a 

N 

c 

•  I-H 

'? 

o 

^— 1 

•iH 

•♦«» 

'o 

03 

^ 

«-t-l 

-M 

Ca 

o 

00 

H 

03 

03 

'd 

J) 
0. 


C/5 

O 

c 


u 
O 

B 

u 

as 

(D 
U 
<U 

o 


O 

6 


to      <^ 


"to    /o 


«a 


-Si 


^ 


Q 
^ 


i  8 

■Si 
<0      -Si 


Co    ^ 
to      ^ 


•^    ^ 

to"     -^ 

"to 
to     "o 


to 
Q    -is 


to 


■♦<» 

«o 


'ti 


G     to 


o 
o 

•^ 


^    S 


^     .       to 


in  '^ 


to 


a. 


Cl. 


to 
<to 


s 

g 

^ 


to 

Q 

to 

O 


t:^ 


"to 

tfc: 

■Si" 


to 

■Ki 


to 

■(~» 
to 


-Si 

Q 


'I- 


•ox, 


% 


'^  -ox, 

2^ 


-Si 


«!i> 
-S 


a    § 


^  f  ^ 
f^  :^  K^ 


^ 
^ 
^ 


u 

Id 


O 


o 


ex, 


to 
S     Co 


s    ^    a 


to     s» 

to     S 


pq 


0) 

CO 

ctS 
O 


o 


lO 

i 

o 

-Si 


^ 
S 
O 


.^  -^  --^ 
^    <^  -^ 

'^     '^      C) 


PL, 

a 

PQ 


en 

a 
O 


o 


(^  "-I  Co  c< 


to 

-Si 

«o 


CM 


f^ 


w-i 


00 


Ov 


O 


o 


o 


^ 

s 


to 

H 


^ 


•Si  .      ^ 

^    r^    ^ 


•♦-4 

§ 

1 

^C> 

^ 

'tf 

-^^ 

«^ 

i»*i 

•^ 

r-^ 

^ 

V. 

o^ 

lo 
O 

to 

^ 

^ 

S 

•<s 

•  ^ 

S 

-iii 

C) 

ca 

-<» 

^ 

•^^A 

-•^ 

Q 

^o 

^ 

•-:i 


o    o    o    c    o    o    o 


to 


S     to 

1^ 


•»      "Si 


to 


to 
to 

5i 


to 


in 
1—1 


u 

pq 

•rH 

o 

U 

pq 


w 
O 

o 


Ss    '^    ^ 


1-* 

to 


^ 


'X3 

t:^ 


-Si 


^O 

§i 


■Si 


to 

t^    ^ 


to 
to 

.     ^ 

Q 

•K4 

a 
tto 


't3 


ca 


to 
to 


h^  ct^  K^  CO  C)  (;) 


to 
to 


o  o  o  o  o  o 


oooooooooo 


O 
to 

1^ 


00 
Q  Co 


Co 
O 

O 
Co 


^  CO  K^  f^  fX,  h. 


Q  S  ^ 
Co   Co   ^ 


«o 

<o 

Co 


to  3 
^  § 
Co 


Co 


Co 


S  ,S  >  ^^  -^ 


Co 


^-,cqcq(/)OQCi,k^[jqkHtq 


s. 

^ 

o 

5» 

to 

-^ 

Q 

^ 

■  ^ 

^ 

V 

<to 

1"^ 

•*.» 

s 

o 

s 

^ 
s 

(^ 

^ 

-§ 

<o 

-Si 

to 

, 

i«» 

t^ 

52 

*^ 

^ 

to 

Q 

S 

•^ 

s 

to 

05 

g 
•^ 

^ 

-^ 

•K4 

■Kk 

to 

e 

to 

1+-^ 

1<i 

■'^ 

Q 

o 

O 

^ 

^ 

^ 

^ 

l*-^ 

e 
s 
^ 

to 

■t^ 

<ii 

^ 

to' 

e  -ii 

O 

►5 

O 

pra- 
ribut 

to 

to 

S 
S 

V 

t^* 

8 

to 

"S 

^ 

8 

t:i 

to 

^ 
^ 

^  ^ 

Q 

^ 

t» 

C) 

H-^ 

ti 

;i 

V    ^ 

^ 

^ 

o 

•'r* 

lysis  and  at 
revis  (Erb' 

tij 

Q    ^ 

'^— . 

^ 

'par 
ator 

Q 

i-*^ 

o  .5^ 

'ti 

§ 

•  .^ 

^  •<<> 

^   ^ 
^    S 

g 
Q 

to 

to 

s    '^ 

« 

io 

1 1 

"^^i 
S 

Q 

$>** 

^ 

?s 

<o 

to 

^•s 

to 

g 

^ 

^ 

•"J^ 

Q 

« 

>v     . 

4:^ 

?^ 

g 

^ 

to 

o 

•^ 

s 

to 

K^     O     <^  H^«  wHi  HfN  whs 
VO     cvj     04     o     O     l>^ 
N      N     H 


^<i     f^    H     H     O     O     t^ 
^    C^l     H      H      H 


^     -5i     ^^     «+>  H->.  H-^ 

^  S  §  -^  .^  -^ 

f^  »-]  ^  O  ^  Co 


to 


--Si    Co 


to 


-^     ta 


«o     ^ 
to 


-§ 

^ 

to 
to 

b^ 

t^ 

tii 

^ 

O 

fe 

^-I 

^4 

^ 

"^ 

Q 

g 

to 

a 

o 

U 

Q 

"tn 


O 

'^ 

H 

M-l 
O 

•  r-l 

be 

•T-t 

a 

(D 


P^ 


CD 

O 

OJ 


O 
u 


CO 


oooooodo 


o   o   o 


to 


(^ 


2^   -O 


^  ^   S   '-3   2 


00      '^ 


ooooooooo 


6 


«o 


<0       CD 


*  -      ^      ^     rs      ^      "Jo 


-       -"^      to 
^     ^     Q 


<^ 


■^ 


a,hiCqco^k!^[5cQ 


o 


O 


o 


^  ^-  ^ 


in 


'^  t3  o  >- 


5^ 


g»      Co 


«o 
to 


o 

u 


Co 
to 


to 


u 
<u    cij 


T3 

o 
o 


b  ^ 
O 


•73 

O 

a 

o 


N 
ts>     rs       *^ 

«0 


c:i 


^ 


■^    to 

►^  ^ 

"^       ^       ii: 

r^  ^  il" 

^  <<;  K< 

si 

•»* 
to 


O 


*o      to 


<i5       tij 

«o      to 


6 

o 
a 

bjo 


be 
•    w 


cj 


o 

u 


«0 


2 


5^ 


li 

-* 

V. 

,2    "^ 

^ 

Ci 

S 

■♦^ 

O 

to 

■^ 

^ 

tr 

t<. 

c^ 

<:» 

<o 

^ 

-^ 

"-^ 

S 
^ 

^0 

1^ 

f^"^ 

^ 

^ 

^ 

o 

§ 

^ 

On 

"^-i 

o 

a 

(^ 

"^ 

<^ 

to 

<o 

g 

ti-O 

^ 

-^ 

<:to 

^0 

.52  f^ 


o 

(^kJ       to 


v. 


Q 


v:> 


•^ 


-  ^ 


;::d  §  1^  b 


Co     to 


■4J  CO 

2  o 

o  S 

a)  O 

Pi  <a 

o  ^ 

to  o 


9?   to 


9.  % 


u 
o  ^ 

Co    jj 


O    1^ 


w 

o 
fl 

^^ 

D      ^     Oj 

;3  ,fl 


m 


CHAPTER  VIII. 

ILLUSTRATIONS    OF    DIAGNOSIS. 

The  following  illustrative  cases  are  placed  here  with  a 
view  to  showing  how  the  methods  of  diagnosis  are  em- 
ployed in  actual  practice.  The  cases  are  for  the  most 
part  typical,  and  present  few  diagnostic  difficulties  but 
some  of  them  deviate  considerably  from  the  common 
types  of  disease,  and  illustrate  some  of  the  difficulties  in 
diagnosis  that  so  frequently  arise. 

I.  A  man  fell  headlong  from  a  scaffold,  a  distance  of  twelve  feet, 
and  at  once  became  paraplegic.  Examination  showed  the  sixth  cer- 
vical vertebra  to  be  somewhat  displaced.  Below  the  arms  there  was 
complete  motor  paralysis  ;  in  the  arms  there  was  complete  paralysis 
of  the  intrinsic  muscles  of  the  hands,  flexors  and  extensors  of  the 
wrists,  and  triceps,  and  partial  paralysis  of  the  biceps,  supinators, 
and  pronators.  There  was  loss  of  sensation  to  pain  or  touch  below  a 
V-shaped  line  across  the  upper  part  of  the  chest,  and,  roughly  speak- 
ing, in  the  inner  half  of  the  arms,  forearms,  and  hands.  It  was  in- 
ferred from  the  distribution  both  of  the  motor  and  the  sensory  loss, 
that  there  was  a  destructive  lesion  of  the  seventh  and  eighth  cervical 
segments  of  the  spinal  cord  (see  pp.  20  and  249).  Above  the  line  of 
sensory  loss  was  an  area  of  hyperalgesia,  which  extended  to  the  lower 
part  of  the  neck.  This  indicated  that  the  fifth  and  sixth  segments  of 
the  cord  were  partially  damaged.  From  the  completeness  of  the 
motor  and  sensory  loss  in  the  parts  below  the  level  of  the  lesion,  it 
was  inferred  that  the  cord  was  destroyed  in  a  large  part  of  its  trans- 
verse extent  at  the  level  of  damage.  The  examination  of  the  reflexes 
confirmed  this  opinion,  for  the  knee-jerks,  cremasteric,  abdominal, 
and  plantar  reflexes  were  abolished,  the  knee-jerks  being  thus  lost  in 
cervical   injuries  only  in  cases  of  severe  damage  to  the  cord.     The 

656   . 


ILLUSTRATIONS   OF  DIAGNOSIS.  657 

bladder  and  rectum  were  emptied  automatically,  which  showed  that 
the  reflex  centres  of  the  cord  for  the  bladder  and  rectum  were  no 
longer  under  cerebral  control. 

The  diagnosis  of  the  nature  of  the  lesion  in  this  case  presented  no 
difficulties.  The  damage  to  the  cord  was  plainly  such  as  could  be 
produced  only  by  the  crushing  effect  of  displacement  of  bone.  The 
fact  that  there  was  only  slight  external  evidence  of  displacement  did 
not  render  this  view  any  less  probable,  because  it  is  common  in  cases 
of  fracture-dislocation  of  the  cervical  spine  for  the  displaced  vertebra 
to  spring  back  at  least  partially  into  place. 

The  patient  died  in  less  than  two  days  after  the  accident,  and  the 
autopsy  confirmed  the  diagnosis.  There  was  a  dislocation  forward  of 
the  sixth  upon  the  seventh  cervical  vertebra,  the  seventh  and  eighth 
cervical  segments  of  the  cord  were  severely  crushed,  and  there  were 
indications  of  slighter  damage  (chiefly  hemorrhage  into  the  central 
canal)  to  the  sixth  and  fifth  segments. 

2.  A  young  man,  aged  twenty-three,  and  of  unusually  strong  build, 
was  suffering  from  a  considerable  degree  of  paralysis  in  the  legs  and 
slighter  paralysis  in  the  arms  when  he  first  came  under  observation. 
Examination  showed  that  the  loss  of  power  in  the  legs  involved  chiefly 
the  anterior  and  posterior  tibial  groups  of  muscles  and  the  extensors  of 
the  knee,  the  adductors  and  abductors  of  the  thigh  and  the  flexors  of 
the  knee  being  involved  in  less  degree.  In  the  upper  extremity  the  loss 
of  power  was  almost  confined  to  the  muscles  of  the  forearm  and  hand, 
the  extensors  of  the  wrist  being  especially  weak.  The  paralyzed 
muscles,  both  in  the  upper  and  lower  extremities,  were  flabby  and 
wasted,  and  showed  the  RD,  the  wasting  and  the  changes  in  irritability 
being  most  pronounced  in  the  muscles  that  were  weakest.  Sensi- 
bility to  touch  and  pain  was  slightly  diminished  below  the  knees. 
Elsewhere  in  the  legs  there  was  a  marked  degree  of  hyperalgesia. 
The  anterior  crural  nerves  were  exceedingly  sensitive  to  pressure. 
The  muscles  of  the  legs  were  very  tender  to  firm  pressure.  From 
time  to  time  there  was  considerable  spontaneous  pain  of  a  shooting 
character  in  the  legs.  In  the  upper  extremities  there  were  no  dis- 
turbances of  cutaneous  sensibility,  but  the  forearm  muscles  were  ten- 
der to  pressure,  and  there  was  some  spontaneous  pain  in  the  arms.  The 
knee-jerks  were  abolished.  The  bladder  and  rectum  were  under  per- 
fect control.  The  patient's  mind  was  clear.  The  temperature  was 
normal.  The  paraplegic  distribution  of  the  symptoms  in  this  case 
immediately  suggested  disease  of  the  spinal  cord  or  peripheral  nerves. 


658        DISEASES   OF   THE   NERVOUS   SYSTEM. 

Spinal  cord  disease  was,  however,  quickly  excluded.  Slow  compres- 
sion of  the  cervical  cord  might  cause  partial  loss  of  power  in  the  upper 
and  lower  extremities,  and  disturbances  of  sensibility,  but  could  not 
be  held  responsible  for  the  muscular  atrophy,  tenderness  of  the  mus- 
cles, and  loss  of  knee-jerk  observed  in  this  case.  A  lesion  in  the 
lumbar  cord  might  account  for  the  loss  of  power,  sensory  disturb- 
ances, wasting,  and  loss  of  knee-jerk,  but  such  a  lesion  would  prob- 
ably involve  the  functions  of  the  bladder  and  rectum,  and  would  cer- 
tainly not  explain  the  symptoms  in  the  upper  extremities.  In  short, 
no  single  lesion  of  the  spinal  cord  would  be  adequate  to  explain  all 
the  symptoms  here  present,  and  the  supposition  of  multiple  lesions 
of  the  cord  was  not  to  be  seriously  considered  until  more  likely  ex- 
planations had  been  sought.  On  the  other  hand,  the  assumption  that 
the  symptoms  were  due  to  a  multiple  affection  of  the  peripheral 
nerves,  afforded  an  explanation  of  the  phenomena  present  that 
was  thoroughly  satisfactory.  The  paralysis,  atrophy,  RD,  sen- 
sory disturbances,  loss  of  knee-jerk,  and  preservation  of  the  functions 
of  the  bladder  and  rectum  could  be  thus  explained.  That  the  process 
in  the  nerves  was  a  neuritis,  was  shown  by  the  tenderness  of  nerve- 
trunks,  the  pain,  the  hyperalgesia,  and  the  tenderness  of  the  muscles. 
The  diagnosis,  then,  as  based  on  the  objective  features  of  the  case, 
was  multiple  neuritis  involving  mixed  nerves  of  both  upper  and  both 
lower  extremities.  Certain  features  of  the  case,  namely  the  slight 
degree  of  anaesthesia,  the  prominence  of  irritative  sensory  symptoms, 
as  pain  and  hyperalgesia,  and  the  tenderness  of  the  muscles,  sug- 
gested the  dependence  of  the  multiple  neuritis  on  alcohol.  This 
inference  was  borne  out  by  the  history.  It  was  learned  that  for  sev- 
eral years  the  patient  had  be'en  in  the  habit  of  using  alcoholic  drinks 
very  freely,  though  never  to  the  extent  of  producing  intoxication.  He 
drank  chiefly  beer,  the  quantity  averaging  from  fifteen  to  twenty 
glasses  a  day.  Until  eight  weeks  before  he  came  under  our  obser- 
vation he  was  in  good  health.  Then  he  began  to  suffer  from  numb- 
ness and  pains  in  the  legs,  to  which  was  soon  added  a  gradual  but 
rather  rapidly  progressive  paralysis,  first  of  the  lower  then  of  the 
upper  extremities.  Thus  the  history  confirmed  the  diagnosis  of 
alcoholic  multiple  neuritis.  The  ultimate  recovery  of  the  patient  was 
another  evidence  of  the  correctness  of  the  diagnosis. 

3.  A  boy,  aged  eighteen,  complained  of  weakness  in  both  lower 
extremities.  It  was  immediately  observed  that  his  gait  was  peculiar. 
Each  leg  was  brought  forward  in  turn  with,  considerable  effort,  and 


ILLUSTRATIONS   OF   DIAGNOSIS.  659 

was  observed  to  be  rigid  and  extended.  Examination  showed  that  the 
loss  of  power  in  the  legs  was  nowhere  considerable  ;  the  weakness  was 
most  marked  in  the  flexors  of  the  thighs,  knees,  and  ankles.  The 
extensors  of  the  knees  showed  no  appreciable  loss  of  power.  In  the 
upper  extremities  power  was  normal.  The  muscles  of  the  legs  were 
the  seat  of  extensor  spasm,  which  was  especially  marked  during  move- 
ment. The  muscles  showed  no  atrophy  or  loss  of  tone  but  were,  on 
the  contrary,  well  developed  and  firm.  The  electrical  reactions  were 
normal.  The  knee-jerks  were  greatly  exaggerated  on  either  side  and 
an  ankle  clonus  was  readily  obtainable.  The  functions  of  the  bladder 
and  rectum  were  normally  discharged. 

It  was  inferred  from  this  combination  of  weakness  and  spasm  in  the 
legs  that  the  case  was  one  of  involvement  of  the  pyramidal  tracts  of  the 
cord.  That  the  lesion  was  confined  to  these  tracts  was  made  probable 
by  the  entire  absence  of  sensory  and  trophic  symptoms.  It  was  learned 
from  the  patient  that  the  spasm  and  weakness  had  come  on  gradually 
during  the  two  preceding  years,  the  symptoms  having  been  at  first 
more  marked  in  the  right  than  in  the  left  leg.  The  apparent  limita- 
tion of  the  process  to  the  pyramidal  tracts  and  the  gradual  and  slow 
development  of  the  symptoms  left  little  doubt  that  the  morbid  process 
was  degenerative  in  nature.  The  case  was,  therefore,  to  be  regarded 
as  one  of  spastic  paraplegia  from  sclerosis  of  the  lateral  pyramidal 
tracts.  But  there  remained  the  question,  is  this  lateral  sclerosis  pri- 
mary or  secondary  ?  Usually  cases  of  lateral  sclerosis  are  secondary 
to  disease  of  the  brain  or  spinal  cord.  There  were  no  evidences 
whatever  of  a  cord  lesion  to  which  a  lateral  sclerosis  might  be  second- 
ary— no  symptoms  suggesting  myelitis,  or  tumor  or  compression  of 
the  cord  from  any  cause.  There  were  no  signs  of  vertebral  disease. 
An  endeavor  was  next  made  to  discover  signs  of  brain  disease,  old  or 
recent.  It  was  observed  that  the  patient  was  mentally  dull,  and  had 
some  hesitation  in  speech,  but  there  were  no  other  cerebral  symptoms. 
The  skull  was  well  developed  and  symmetrical.  There  was  no  stra- 
bismus or  nystagmus.  The  patient  was  free  from  headache.  Inquiry 
into  the  history  of  the  case  likewise  failed  to  give  evidence  of  cerebral 
disease.  There  was  no  history  of  traumatism  during  birth  or  of  con- 
vulsive seizures  during  infancy  or  childhood,  and,  as  already  stated, 
the  symptoms  of  spinal  cord  disease  did  not  begin  until  two  years 
before  the  patient  came  under  observation.  As  no  evidences  could  be 
obtained  of  brain  or  cord  disease  to  which  degeneration  of  the  lateral 
tracts  might  be  secondary,  the  case  was  regarded  as  one  of  primary 


66o         DISEASES   OF   THE   NERVOUS   SYSTEM. 

lateral  sclerosis.  It  must  be  admitted,  however,  that  this  diagnosis 
was  not  perfectly  satisfactory.  The  mental  retardation  and  speech 
disturbance  remained  unaccounted  for  ;  and  as  cases  of  unquestionable 
primary  lateral  sclerosis  are  of  very  rare  occurrence  as  compared  with 
cases  of  secondary  lateral  sclerosis,  the  possibility  that  the  process  was 
in  this  case  secondary  to  an  old  and  obscure  cerebral  lesion  could  not 
be  entirely  excluded. 

4.  A  boy,  aged  ten,  slipped  upon  the  ice  and  fell  to  the  ground  in 
the  sitting  posture.  He  walked  to  his  home,  which  was  some  distance 
away,  and  after  several  hours  began  to  complain  of  weakness,  numb- 
ness and  pain  in  his  legs.  Examination  about  twenty-four  hours  after 
the  fall  showed  complete  loss  of  power  below  the  knees  and  consid- 
erable weakness  of  the  thigh  and  hip  muscles.  Sensation  was  un- 
impaired but  for  numbness  and  tingling  in  the  legs.  The  knee-jerks 
were  abolished,  and  there  was  incontinence  of  urine  and  faeces.  There 
was  a  slight  elevation  in  temperature.  In  the  course  of  a  few  days  the 
muscles  of  the  thighs  and  hips  lost  all  power,  and  the  tactile  and  pain 
senses  were  abolished  below  a  transverse  line  a  short  distance  above 
the  pubes.  The  plantar  and  cremasteric  reflexes  were  lost  at  this  time, 
but  the  abdominal  reflex  was  preserved.  There  was  still  a  slight  rise 
in  temperature. 

The  diagnosis  of  the  position  of  the  lesion  in  this  case  presented  no 
difficulties.  The  initial  loss  of  power  in  the  legs,  the  abolition  of  the 
knee-jerks,  and  the  paralysis  of  the  sphincters  indicated  clearly  that 
the  structures  in  the  lower  part  of  the  lumbar  enlargement  which 
subserve  motion  and  the  visceral  and  tendon  reflexes  were  the  seat  of 
disease.  The  initial  preservation  of  sensibility  in  the  legs  made  it 
probable  that  the  damage  was  limited  chiefly,  if  not  entirely,  to  the 
motor  structures  of  the  cord.  The  subsequent  loss  of  sensibility  in 
the  legs  and  the  ascent  of  the  motor  paralysis  to  the  flexors  and  exten- 
sors of  the  thigh  led  to  the  inference  that  there  had  been  an  increase 
both  in  the  transverse  and  vertical  extent  of  the  lesion.  The  com- 
pleteness of  the  motor  and  sensory  loss  made  it  probable  that  the 
lesion  involved  the  greater  part  of  the  transverse  extent  of  the  cord. 
The  vertical  extent  of  the  lesion  was  inferred  from  the  distribution  of 
the  paralysis  and  the  state  of  the  various  reflexes.  The  paralysis  of 
the  rectal  sphincter,  the  loss  of  sensibility  over  the  perineum,  and  the 
loss  of  plantar  reflex  showed  that  the  cord  was  involved  as  low  as  its 
sacral  segments.  The  loss  of  cremasteric  reflex  showed  that  the  cord 
was  involved  as  high  at  least  as  the  first  or  second  lumbar  segments 


ILLUSTRATIONS   OF  DIAGNOSIS.  66l 

That  the  lesion  did  not  extend  much  higher  than  this  was  inferred 
from  the  preservation  of  the  abdominal  reflex,  which  depends  on  the 
integrity  of  the  dorsal  nerves  from  the  seventh  to  the  twelfth,  and 
also  from  the  transition  to  normal  sensibility  a  short  distance  above 
the  pubes. 

The  diagnosis  of  the  nature  of  the  lesion  was  less  simple.  The 
extension  and  progress  of  the  motor  and  sensory  symptoms  and  the 
presence  of  fever  made  it  certain  that  the  lesion  soon  became  inflam- 
matory in  character,  whatever  may  have  been  its  original  character. 
It  was  believed  by  some  that  the  initial  lesion  was  hemorrhage  into 
the  gray  matter  of  the  cord,  but  the  facts  that  the  symptoms  did  not 
come  on  for  several  hours  after  the  fall,  and  that  they  developed  rap- 
idly but  not  suddenly,  made  it  more  probable  that  the  lesion  was  from 
the  first  an  inflammation.  The  diagnosis  of  lumbar  myelitis  was 
confirmed,  if  such  confirmation  was  needed,  by  the  subsequent  course 
of  the  case.  The  paralyzed  muscles  atrophied  greatly,  and  showed 
the  RD,  bed-sores  formed,  and  the  patient  at  length  died  of 
exhaustion. 

5.  A  man,  aged  thirty-two,  presented  himself  with  inco-ordination 
and  weakness  in  the  lower  extremities.  Both  these  symptoms  were 
apparent  in  his  gait.  As  the  patient  progressed  unsteadily  across  the 
floor,  his  feet  were  lifted  high  and  brought  to  the  ground  with  an 
irregular  flap.  A  slight  degree  of  dropping  of  the  feet  from  weak- 
ness of  the  anterior  tibial  groups  of  muscles  was  also  observable. 
Examination  showed  slight  inco-ordination  of  the  upper  extremities, 
but  no  weakness.  In  the  legs  there  was  a  high  degree  of  inco- 
ordination, and  the  patient  was  unable  to  stand  with  his  eyes  closed. 
The  loss  of  power  in  the  legs  appeared  to  be  confined  to  the  anterior 
tibial  and  peroneal  groups  of  muscles,  but  the  patient  said  he  felt 
weak  also  in  the  knees.  The  anterior  tibial  and  peroneal  muscles 
showed  a  slight  degree  of  atrophy  and  a  partial  form  of  RD.  The 
posterior  tibial  group  showed  partial  RD,  but  no  appreciable  weak- 
ness or  wasting.  Sensibility  was  normal  except  on  the  soles  and 
backs  of  the  feet,  where  there  was  slight  anaesthesia  and  analgesia. 
There  were  paraesthesise  in  other  parts  of  the  legs,  and  from  time  to 
time  considerable  sharp  pain.  The  knee-jerks  were  abolished  on 
both  sides. 

By  far  the  most  obtrusive  symptom  in  this  case  was  the  inco- 
ordination. A  high  degree  of  inco-ordination  may  be  of  cerebrai, 
spinal,  or  peripheral  origin.     In  this  case  there  was  nothing  to  suggest 


662        DISEASES   OF   THE   NERVOUS   SYSTEM. 

brain  disease.  The  associated  loss  of  power  in  the  leg§,  the  atrophy, 
the  RD,  the  disturbances  of  sensibility,  and  the  loss  ot  knee-jerks, 
all  indicated  that  the  lesion  was  one  of  the  cord  or  peripheral  nerves. 
A  lesion  of  the  posterior  columns  of  the  cord  and  posterior  root-zones 
would  explain  the  presence  of  inco-ordination,  pains  in  the  legs, 
slight  anaesthesia,  and  loss  of  knee-jerks.  A  lesion  of  these  structures 
almost  invariably  depends  on  a  degenerative  process,  and  then  gives 
rise  to  the  clinical  picture  of  locomotor  ataxia.  But  the  diagnosis  of 
locomotor  ataxia  did  not  afford  a  full  explanation  of  the  symptoms, 
in  this  case  ;  it  did  not  explain  the  presence  ot  weakness,  wasting, 
and  altered  electrical  reactions.  These  symptoms  might  depend 
either  on  a  limited  lesion  of  the  ganglion  cells  of  the  anterior  horns  in 
the  middle  of  the  lumbar  enlargement,  or  on  disease  of  the  motor 
fibres  originating  in  these  structures  and  forming  part  of  the  pe- 
ripheral nerves.  The  former  condition  is  not  an  associated  lesion  of 
locomotor  ataxia  ;  the  latter  frequently  is.  All  the  symptoms,  then, 
might  be  explained  on  the  supposition  that  we  had  to  deal  with  a 
case  of  locomotor  ataxia  with  associated  changes  (neuritis)  in  certain 
peripheral  nerves.  But  this  is  not  the  only  condition  that  would 
account  for  the  symptoms.  As  intimated  above,  the  inco-ordination 
present  might  depend  on  a  lesion  limited  exclusively  to  the  peripheral 
nerves.  Such  a  lesion,  involving  both  the  motor  and  sensory  fibres 
of  mixed  nerves,  would  explain  satisfactorily  not  only  the  inco- 
ordination but  also  the  weakness,  atrophy,  RD,  loss  of  knee-jerks, 
and  sensory  symptoms.  In  short,  the  symptoms  of  the  case  might 
be  satisfactorily  explained  either  by  a  locomotor  ataxia  with  associ- 
ated neuritis  or  by  a  multiple  neuritis  alone.  The  distinction  between 
these  conditions  could  not  be  made  from  the  facts  gathered  by  the 
examination  of  the  patient.  It  therefore  became  necessary  to  see 
what  bearing  the  history  of  the  case  might  have  upon  the  diagnosis. 
It  was  learned  that  six  months  before  the  date  of  examination  the 
patient  was  in  fair  general  health.  He  then  began  to  lose  flesh  and 
suffered  from  numbness,  tingling,  and  sharp  pains  (never  very  severe) 
in  the  legs.  In  a  few  months  he  grew  unsteady  in  walking  and 
developed  some  weakness  in  the  legs.  Both  these  symptoms  increased 
rather  rapidly.  Ten  years  ago  the  patient  had  a  hard  chancre  and 
during  the  two  years  previous  to  examination  had  used  alcohol  in  great 
excess.  The  history  of  excessive  use  of  alcohol  before  the  onset  of 
the  symptoms  rendered  an  alcoholic  neuritis  a  probable  condition  ;  the 
clear  history  of  a  hard   chancre  would  explain  the  presence  of  loco- 


ILLUSTRATIONS   OF   DIAGNOSIS.  663 

motor  ataxia.  The  facts  of  etiology,  therefore,  did  not  aid  in  solving 
the  diagnostic  problem.  But  the  following  facts  all  pointed  to  the 
presence  of  alcoholic  neuritis  rather  than  locomotor  ataxia  :  the 
relative  youth  of  the  patient  (thirty-two  years),  the  development  of 
all  the  symptohis  within  so  short  a  time  as  six  months,  the  absence  of 
very  severe  fulgurating  pains,  and  the  absence  of  all  ocular  symptoms 
— especially  the  absence  of  the  Argyll-Robertson  pupil. 

This  diagnosis  was  made  with  some  caution,  but  was  considered 
highly  probable  by  several  skilled  physicians.  It  has  not  been  borne 
out  by  time.  A  year  has  elapsed  since  the  patient  first  came  under 
notice,  but  there  has  been  little  or  no  Improvement  in  the  symptoms 
and  the  pains  have  been  more  severe  than  before.  The  diagnosis,^ 
therefore,  still  remains  uncertain. 

6.  A  man,  aged  thirty-three,  complained  of  pain  in  his  right  arm. 
Inspection  showed  that  the  extensors  of  the  wrist  were  paralyzed  and 
gave  rise  to  pronounced  wrist-drop.  The  flexors  of  the  wrist  showed 
some  apparent  loss  of  power  owing  to  the  dropping  of  the  wrist, 
but  there  was  no  actual  paralysis.  The  muscles  on  the  back  of  the 
forearm  were  considerably  atrophied  and  showed  the  RD.  Sensibility 
was  unimpaired.  The  limitation  of  paralysis  and  degenerative  atrophy 
to  the  extensors  of  the  wrist  on  one  side  immediately  suggested  the 
dependence  of  these  syinptoms  on  a  lesion  of  the  musculo-spiral 
nerve.  The  power  of  the  supinator  longus  muscle  was  then  tested, 
and  it  was  found  to  be  somewhat  diminished.  It  also  showed  a 
diminution  in  faradic  irritability,  and  equal  and  somewhat  sluggish 
polar  reactions  to  the  galvanic  current.  These  observations  tended 
to  confirm  the  diagnosis  of  musculo-spiral  paralysis.  The  history  of 
the  case  was  next  considered  with  a  view  to  its  bearing  on  this 
diagnosis.  Careful  inquiry  was  made  for  some  cause  of  pressure  on 
the  musculo-spiral  nerve,  but  none  could  be  found.  It  was  learned 
that  the  paralysis  had  come  on  in  the  course  of  a  few  days,  and  that 
it  had  now  lasted  several  weeks.  It  was  also  learned  that  for  some 
weeks  before  the  paralysis  appeared  there  had  been  pains  in  both 
forearms.  The  patient  was  a  painter  and  had  recently  been  much 
exposed  to  lead  in  "flatting."  These  facts  strongly  suggested  the 
dependence  of  the  paralysis  on  lead,  but  the  apparently  unilateral 
distribution  of   the  palsy,   together  with  the  absence  of  a  lead  line 

^  This  case  illustrates  well  the  difficulties  of  diagnosis.  The  correct  diagnosis 
was  of  much  importance  in  this  case,  as  the  prognosis  is  very  different  in  the  two 
forms  of  disease. 


664         DISEASES   OF   THE   NERVOUS  SYSTEM. 

or  a  history  of  colic,  rendered  lead  palsy  improbable.  A  more  care- 
ful examination  was  now  made  of  the  left  arm.  Slight  weakness 
was  soon  detected  in  the  extensors  of  the  wrist  and  an  electrical 
examination  showed  a  decided  diminution  of  faradic  irritability  in 
these  muscles.  The  discovery  of  involvement  of  the  extensors  of 
the  left  arm,  slight  though  it  was,  entirely  altered  the  aspect  of 
the  case.  The  bilateral  extensor  paralysis,  preceded  by  slight 
sensory  symptoms  and  occurring  in  a  painter,  made  it  evident 
that  the  case  was  one  of  lead  neuritis.  The  unequal  involvement 
of  the  muscles  of  the  two  sides  is  an  unusual  feature  of  lead  paralysis. 
The  slight  loss  of  power  in  the  supinator  longus  of  the  right  side  did 
not  militate  against  the  diagnosis,  for  such  partial  involvement  of 
the  supinator  is  not  rare  in  lead  jmlsy. 

7.  A  boy,  aged  ten  years,  came  under  my  observation  on  account 
of  the  frequently  repeated  epileptiform  seizures  to  which  he  was  sub- 
ject. Inspection  showed  the  patient  to  be  much  below  the  average 
size  of  boys  of  his  own  age — his  twin  brother  was  about  four  inches 
taller  and  correspondingly  larger.  The  walk  of  the  patient  was 
exceedingly  unsteady,  and  showed  considerable  weakness  in  the  lower 
extremities  ;  there  was  a  high  grade  of  mental  weakness  (imbecility), 
and  only  monosyllabic  speech.  Examination  showed  all  four  extremi- 
ties to  be  small  and  imperfectly  developed.  The  weakness  in  the  legs 
was  not  confined  to  a  particular  group  of  muscles,  but  involved  the 
leg  as  a  whole.  The  extensors,  however,  were  very  slightly  affected. 
The  muscles,  though  small,  showed  no  indication  of  atrophy.  Their 
tone  was  normal  or  even  greater  than  normal,  there  being  slight  ex- 
tensor spasm  at  times.  The  electrical  reactions  were  normal.  Both 
knee-jerks  were  much  exaggerated.  The  skin  reflexes  were  all  active. 
Ankle  clonus  could  not  be  obtained.  In  the  upper  extremity  there 
was  a  well  marked  intention  tremor.  Sensibility  was  everywhere 
normal.  The  head  was  abnormally  small  and  the  palate  was  high- 
arched.  The  prominent  features  of  this  case  were  the  mental  weak- 
ness, the  evidences  of  arrest  of  development  in  the  extremities  and  in 
the  cranium,  the  occurrence  of  epileptiform  attacks,  and  the  weakness 
and  spasm  in  the  legs.  All  of  these  conditions  indicated  the  pres- 
ence of  a  cerebral  lesion.  Certain  of  the  symptoms,  as  weakness  and 
spasm  in  the  legs,  occurring  by  themselves  would  suggest  spinal  cord 
disease  rather  than  a  cerebral  process,  but  with  the  associations  above 
mentioned  these  symptoms  indicate  a  cerebral  and  not  a  spinal  cord 
lesion.     The  bilateral  distribution  of  the  symptoms  and  their  involve- 


ILLUSTRATIONS   OF   DIAGNOSIS.  665 

ment  of  the  arms  as  well  as  the  legs,  indicated  that  the  motor  path 
was  implicated  in  a  considerable  part  of  its  extent  in  bot'~  hemi- 
spheres of  the  brain.  The  signs  of  retarded  development,  both  mental 
and  physical,  made  it  plain  that  the  morbid  process  was  one  of  long 
duration,  in  fact  that  it  must  have  commenced  in  infancy  or  early 
childhood.  Cerebral  palsies  at  this  time  of  life  are  either  congenital 
or  acquired,  the  congenital  form  being  generally  dependent  upon 
injury  during  birth,  the  acquired  form  depending  on  a  variety  of  dif- 
ferent conditions  in  different  cases  (see  p.  367).  It  was  impossible  to 
say  with  certainty  in  which  of  these  catagories  the  case  belonged,  with- 
out taking  into  consideration  the  history  of  the  case.  But  the  pres- 
ence of  a  high  grade  of  niental  defect,  the  physical  evidences  of  con- 
siderable retardation  of  growth,  and  the  bilateral  and  symmetrical 
distribution  of  the  symptoms  suggested  that  the  condition  was  a  birth 
palsy.  This  view  was  corroborated  by  the  history  of  the  case.  It 
was  learned  that  the  patient  was  the  first  child  born  in  a  twin  labor, 
that  the  mother  was  at  that  time  a  primipara,  that  the  second  stage  of 
labor  lasted  nearly  twenty  hours,  and  that  the  child  had  several 
general  convulsions  during  the  hour  following  delivery.  These  con- 
vulsions were  frequently  repeated  during  the  first  months  of  life  and 
had  continued,  with  decreasing  frequency,  ever  since.  These  facts 
were  a  perfect  confirmation  of  the  diagnosis,  and  removed  any  doubts 
as  to  the  nature  of  the  lesion,  which  could  have  been  nothing  else 
than  a  meningeal  hemorrhage,  extending  over  both  convexities,  result- 
ing eventually  in  a  sclerosis  and  atrophy  of  the  parts  of  the  cortex  and 
subcortical  substance  involved  and  secondary  degeneration  of  the 
pyramidal  tracts. 

8.  A  child,  three  years  of  age,  came  under  observation  suffering 
from  paralysis  in  both  lower  extremities  and  partial  loss  of  power 
in  the  right  arm.  There  were  typical  athetoid  movements  in 
the  fingers  of  the  right  hand,  with  temporary  flexor  spasm,  moderate 
atrophy  of  the  forearm  muscles,  and  slight  loss  of  power.  Thefaradic 
irritability  of  the  forearm  muscles  was  slightly  diminished,  but  there 
was  no  RD  in  any  muscles  of  the  upper  extremity.  Sensibility  was 
nowhere  affected.  These  conditions  in  the  upper  extremity  at  once 
suggested  a  cerebral  palsy,  and  this  idea  was  strengthened  by  observa- 
tion that  the  patient  was  backward  in  intelligence  and  speech.  The 
lower  extremities  were  next  examined  to  see  whether  their  condition 
corroborated  the  diagnosis  of  a  cerebral  palsy.  There  was  a  high 
grade  of  paralysis  of  all  the  muscles  of  the  legs  except  the  flexors  of 


666        DISEASES   OF   THE   NERVOUS   SYSTEM. 

the  hips,  the  paralyzed  muscles  were  greatly  atrophied  and  flabby,  and 
showed  the  RD.  Below  the  knees  the  paralysis  was  absolute  and  the 
feet  were  in  equinus.  The  knee-jerks  were  lost.  The  sphincters 
were  unaffected.  Sensibility  was  everywhere  normal  in  the  lower 
extremities.  The  extremities  were  cold  and  the  color  of  the  skin 
showed  defective  circulation. 

The  presence  of  a  high  grade  of  paralysis  and  atrophy  in  the  legs, 
the  reaction  of  degeneration  in  the  paralyzed  muscles,  and  the  loss  of 
knee-jerks  all  pointed  to  the  existence  of  a  lesion  of  the  lumbar  en- 
largement, involving  the  ganglion-cells  of  the  anterior  horns.  That 
the  lesion  was  confined  to  these  motor  structuies  was  shown  by  the 
fact  that  only  the  trophic,  motor,  and  reflex  functions  of  the  cord  were 
impaired,  the  various  forms  of  sensibility  being  intact.  The  same 
case  therefore  presented  unmistakable  evidences  of  two  quite  distinct 
lesions,  one  involving  the  motor  path  in  the  brain,  probably  in  the 
cortex  or  subcortical  region,  the  other  involving  motor  ganglion- 
cells  in  the  lumbar  enlargement  of  the  cord.  The  cord  symptoms 
were  of  the  kind  observed  in  an  advanced  stage  of  acute  poliomyelitis. 
Further  indications  as  to  the  nature  of  the  lesions  in  the  brain  and 
cord  were  derived  from  a  consideration  of  the  onset  of  the  symptoms. 
It  was  learned  from  the  mother  of  the  patient  that,  one  year  before  the 
child  came  under  observation,  it  became  restless  and  feverish  for  sev- 
eral days,  and  at  the  end  of  this  became  delirious,  had  high  fever,  and 
vomited  repeatedly.  During  this  latter  period  of  acute  illness  there 
were  repeated  clonic  spasms  in  the  right  arm  and  leg,  strabismus,  and 
ptosis.  The  one-sided  convulsions  lasted  about  two  days  and  then 
the  rigid  arm  was  noticed  to  be  without  power.  The  mother  was 
uncertain  as  to  the  state  of  the  right  leg  at  this  time,  but  believes  it 
was  little  or  not  at  all  weak.  Five  days  after  the  onset  of  the  convul- 
sions it  was  observed  that  there  was  complete  loss  of  power  in  both 
legs.  There  was  gradual  recovery  of  power  in  the  right  arm,  but 
little  or  no  improvement  in  power  in  the  legs,  which  soon  wasted. 
With  this  history  there  could  be  little  doubt  that  both  the  cerebral  and 
the  spinal  cord  lesion  were  dependent  on  similar  morbid  processes, 
infectious  in  origin,  and  giving  rise  in  the  one  case  to  an  acute  corti- 
cal lesion  in  the  left  motor  region  (polio-encephalitis,  thrombosis  of 
cerebral  veins?),  in  the  other  to  an  acute  anterior  poliomyelitis.  Cases 
similar  to  this  one  are  very  rare,  but  are  instructive  as  illustrating  the 
relationship  in  etiology  between  some  cases  of  acquired  infantile 
cerebral  palsy  and  anterior  poliomyelitis. 


ILLUSTRATIONS   OF  DIAGNOSIS.  66^ 

9.  A  girl,  aged  nine,  was  suffering  from  partial  paralysis  of  the 
right  arm  and  right  leg  when  she  first  came  under  observation.  In 
the  leg  the  paralysis  was  of  slight  degree  and  involved  about  equally 
all  the  muscles  of  the  limb.  In  the  arm  the  degree  of  weakness 
was  greater,  and  there  was  a  well  marked  contracture  of  the  flexors 
of  the  forearm.  The  face  was  uninvolved.  There  was  no  atrophy 
of  the  affected  muscles,  and  sensibility  was  everywhere  normal. 
The  hemiplegic  distribution  of  the  weakness  in  this  case  suggested 
the  dependence  of  the  paralysis  on  a  cerebral  lesion.  Some  support 
was  lent  this  view  by  the  fact  that  there  was  internal  strabismus  of 
the  left  eye,  such  as  often  remains  after  an  infantile  cerebral  palsy. 
Moreover,  the  knee-jerk  was  greatly  exaggerated  on  the  paralytic 
side  and  unchanged  on  the  normal  side,  and  this  indicated  a  secon- 
dary degeneration  of  the  pyramidal  tracts  on  the  paralytic  side, 
such  as  usually  follows  a  cerebral  palsy.  But,  on  the  other  hand, 
certain  facts  about  the  case  failed  to  confirm  the  diagnosis  of  a 
cerebral  palsy,  and  even  tended  to  disprove  it.  First  there  was  no 
loss  whatever  in  mental  power.  The  patient  was,  on  the  contrary, 
highly  intelligent  and  well  developed  mentally.  Such  entire  immu- 
nity from  mental  defect  is  unusual  in  infantile  cerebral  palsies  which 
give  rise  to  a  considerable  degree  of  permanent  paralysis.  Sec- 
ondly, there  were  no  evidences  of  arrest  of  development  in  the 
affected  limbs,  and  such  evidences  are  almost  always  present  in 
cerebral  palsies  of  children  if  the  paralysis  has  endured  a  consid- 
erable length  of  time. 

An  inquiry  into  the  history  of  the  case  soon  did  away  with  any 
doubts  as  to  the  position  and  nature  of  the  lesion.  It  was  learned 
that  the  child  had  been  perfectly  well  until  she  was  seven  years  of 
age  (or  two  years  before),  and  that  she  then  developed  weakness  in 
both  legs.  This  weakness  slowdy  increased  in  the  legs  and  extended 
to  the  arms,  so  that  at  the  end  of  six  months  there  was  complete 
paralysis  of  motion  below  the  neck.  There  was  also  entire  loss  of 
sensation  below  the  neck.  The  muscles  of  the  neck  had  meanwhile 
grown  weak,  and  the  patient  was  unable  to  keep  the  chin  from  resting 
on  the  neck.  She  was  kept  quiet  in  the  recumbent  position  for  many 
months,  and  gradually  the  anaesthesia  wore  away.  Then  there  was 
a  gradual  return  of  power  in  the  legs  and  left  arm,  but  the  right  arm 
continued  weak.  In  course  of  time  the  muscles  of  the  neck  regained 
full  power.  The  paraplegia  could  have  been  due  only  to  disease  of 
the  upper  cervical  region  of  the  cord,  and  the  gradual  onset  of  the 


668         DISEASES   OF  THE   NERVOUS   SYSTEM. 

symptoms  and  recovery  after  a  period  of  recumbency  left  no  doubt 
that  the  lesion  was  a  compression  of  the  cord  from  caries  of  the 
upper  cervical  vertebrae.  At  the  time  when  the  patient  came  under 
observation  there  were  no  evidences  whatever  of  disease  of  the  cer- 
vical vertebrae,  and  the  conditions  bore  no  little  resemblance  to  those 
observed  in  cerebral  palsies.  The  strabismus,  it  was  learned,  was 
present  many  years  before  the  development  of  nervous  symptoms 
and  therefore  had  nothing  to  do  with  these  symptoms.  It  is  doubt- 
ful whether  a  correct  diagnosis  could  have  been  made  in  this  case 
without  some  knowledge  of  the  previous  history. 

lo.  A  man,  aged  fifty-four,  complained  for  several  days  of  head- 
ache and  slight  numbness  in  the  left  extremities,  and  soon  after 
arising  one  morning  became  rapidly  hemiplegic.  The  loss  of  power 
involved  the  left  leg,  left  arm,  and  left  side  of  the  face  in  its  lower 
part.  There  was  no  loss  of  consciousness  at  the  time  of  the  onset, 
but  the  patient  felt  giddy  and  had  considerable  headache.  When 
examined,  about  twenty-four  hours  after  the  onset  of  the  hemiplegia, 
the  patient  was  in  a  state  of  stupor  from  which  he  could  be  partially 
aroused.  Temperature,  ioo°  Fah.  ;  pulse,  80;  radial  arteries, 
atheromatous  ;  respiration,  20,  regular.  There  was  complete  left 
hemiplegia,  and  the  arm  and  leg  muscles  were  quite  relaxed.  Sensi- 
bility was  diminished  in  the  extremities  in  their  distal  portions. 
The  knee-jerk  was  greatly  diminished  on  the  left  side,  normal  on 
the  right.  The  pupils  were  equal  and  moderately  large.  There  was 
no  spasm  or  other  irritative  symptoms. 

The  diagnosis  of  the  position  of  the  lesion  was  not  difficult. 
Complete  left-sided  hemiplegia  might  result  from  a  lesion  in  the 
right  motor  path  anywhere  between  the  motor  cortex  and  the  upper 
half  of  the  pons.  The  absence  of  spasm  made  it  exceedingly  im- 
probable that  the  lesion  was  cortical  or  subcortical,  and  there  was 
nothing  to  indicate  a  lesion  of  the  crus.  It  was  therefore  highly 
probable  that  the  lesion  was  in  the  right  internal  capsule — the  seat 
of  damage  in  most  cases  of  sudden  hemiplegia.  The  diagnosis  of 
the  nature  of  the  lesion  was  less  easy.  A  sudden  hemiplegia  usually 
depends  on  hemorrhage  or  acute  softening.  Acute  softening  is  gen- 
erally due  to  thrombosis  from  atheroma  or  from  syphilitic  endarte- 
ritis, or  to  embolism.  Embolism  was  excluded  because  there  were 
no  evidences  of  heart  disease,  and  because  there  were  distinct  pre- 
monitory symptoms  before  the  onset  of  the  hemiplegia.  Thrombo- 
sis from  atheroma  was   considered    improbable  on  account   of  the 


ILLUSTRATIONS   OF  DIAGNOSIS.  669 

age  of  the  patient.  Either  cerebral  hemorrhage  or  thrombosis  from 
syphilitic  endarteritis  would  explain  the  symptoms,  and  between 
these  two  conditions  it  was  difficult  to  decide.  The  facts  which 
favored  the  supposition  of  hemorrhage  were  the  age  of  the  patient 
and  the  presence  of  atheroma  of  the  accessible  arteries.  The  facts 
favoring  syphilitic  endarteritis  were  the  presence  of  distinct  pre- 
monitory symptoms  (headache,  numbness,  slight  weakness)  for 
several  days  before  the  onset,  and  the  absence  of  loss  of  con- 
sciousness. These  facts  also  weighed  against  the  diagnosis  of 
hemorrhage,  for  in  hemorrhage  true  premonitory  symptoms  are 
rare,  and  a  capsular  hemorrhage  sufficiently  large  to  produce  com- 
plete hemiplegia  would  almost  certainly  have  given  rise  to  loss  of 
consciousness.  Although  no  history  of  syphilis  could  be  obtained, 
several  tubercles  were  observed  on  the  upper  part  of  the  chest, 
which  had  the  appearance  of  gummata.  On  the  whole,  therefore, 
the  facts  of  the  case  pointed  to  acute  softening  from  syphilitic  endar- 
teritis rather  than  to  hemorrhage.  The  patient  was  put  on  large 
doses  of  iodide  of  potassium,  and  in  time  made  a  good  recovery.  In 
about  two  weeks  from  the  time  of  the  onset  he  had  largely  recov- 
ered power  in  the  hemiplegic  parts  and  the  headache  had  grown  much 
less  severe.  Eventually  gross  power  was  entirely  regained,  but  there 
remained  some  awkwardness  in  executing  the  finer  movements  of  the 
fingers.  Slight  attacks  of  giddiness  occurred  from  time  to  time  after 
recovery  of  power,  and  the  knee-jerk  became  greatly  exaggerated  on 
the  left  side.  There  also  developed  an  ankle  clonus  on  this  side.  It 
was  learned  many  months  after  the  attack  that  the  patient  had  had  a 
chancre  several  years  before.  About  eighteen  months  after  the 
hemiplegia  the  wife  of  the  patient  came  under  observation  for  an 
abundant  syphilitic  eruption  over  both  legs.  These  facts  all  con- 
firmed the  diagnosis  of  the  nature  of  the  lesion  underlying  the 
hemiplegia. 

II.  A  woman,  aged  thirty-four,  was  admitted  to  the  hospital  in  a 
condition  of  stupor  and  with  slight  elevation  of  temperature.  About 
two  inches  above  the  root  of  the  nose  and  just  a  little  to  the  left  of 
the  median  line  was  a  suppurating  incised  wound.  Examination 
showed  that  the  frontal  bone  was  fractured  just  beneath  the  wound. 
The  patient  could  be  roused  for  a  moment  from  her  stupor,  and  at 
times  uttered  partially  intelligible  monosyllables  when  so  aroused. 
The  eyes  had  a  fixed,  staring  expression.  At  times  the  left  hand 
was  placed  on  the  head  while  the  patient  groaned  with  pain.     The 


6/0       DISEASES   OF   THE   NERVOUS   SYSTEM. 

temperature  was  loi  ".  There  was  nothing  noteworthy  about  the 
pulse  or  respiration.  The  pupils  were  equal,  of  moderate  size,  and 
reacted  to  light.  There  was  incomplete  ptosis  of  the  left  lid.  The 
right  arm  was  almost  completely  paralyzed  ;  the  right  leg  was  less 
completely  paralyzed.  The  right  arm  was  constantly  rigid  ;  no 
spasm  elsewhere.  There  was  general  hyperaesthesia.  On  the  right 
side  there  was  great  exaggeration  of  the  knee-jerk  and  violent  and 
prolonged  ankle  clonus.  On  the  left  side  the  knee-jerk  was  in- 
creased, but  ankle  clonus  could  be  obtained  only  with  difficulty. 
There  was  entire  loss  of  control  over  the  sphincters. 

The  presence  of  loss  of  power  in  the  right  arm  and  partial  loss  of 
power  in  the  right  leg,  with  exception  of  the  face,  made  it  certain 
that  there  was  a  lesion  in  the  left  motor  path.  A  lesion  involving 
the  cortex  might  give  rise  to  such  a  partial  hemiplegia  but  would 
produce  more  decided  irritative  symptoms  than  were  here  present.  A 
lesion  in  the  internal  capsule  or  in  the  motor  path  below  the  internal 
capsule  would  not  be  apt  to  exempt  the  face  unless  the  lesion  were 
very  small.  But  a  lesion  between  the  cortex  and  the  internal  capsule 
might  be  of  considerable  size  and  nevertheless  involve  chiefly  the  path 
to  the  arm  of  the  opposite  side,  and  such  a  lesion  would  not  be  apt 
to  cause  clonic  spasm.  It  was  upon  the  whole  probable,  therefore, 
that  the  lesion  was  one  of  the  subcortical  white  substance  of  the  left 
motor  path.  The  diagnosis  of  the  nature  of  the  lesion  could  be  de- 
termined with  less  certainty.  The  limitation  of  the  paralysis  to  the 
parts  above-mentioned  and  the  completeness  of  the  motor  loss  made 
it  probable  that  the  lesion  was  destructive  in  character.  Such  a 
lesion  might  be  a  vascular  lesion,  or  an  inflammatory  lesion,  or  a  new 
growth.  But  it  was  known  that  the  symptoms  were  not  of  sudden 
onset,  and  hence  a  vascular  lesion  was  out  of  the  question.  The 
presence  of  fever  made  it  likely  that  the  lesion  was  inflammatory  in 
nature.  It  could  scarcely  be  meningitis,  for  mere  meningitis  would 
not  give  rise  to  such  complete  and  definitely  limited  paralysis,  and 
would  cause  more  decided  irritative  symptoms  than  were  here  present. 

An  abscess,  however,  would  be  competent  to  cause  a  local  paraly- 
sis, would  not  necessarily  be  accompanied  with  irritative  symptoms 
and  would  almost  certainly  be  attended  with  fever.  The  presence  of 
a  neglected  compound  fracture  of  the  frontal  bone  offered  a  sufficient 
explanation  for  the  occurrence  of  abscess. 

The  patient  died  in  a  few  days  without  developing  any  new  symp- 
toms of  importance.    The  autopsy  showed  the  presence  of  an  abscess 

39 


ILLUSTRATIONS   OF   DIAGNOSIS.  6/1 

of  the  left  frontal  lobe,  which  contained  from  two  to  three  ounces  of 
pus.  The  abscess  extended  back  to  and  somewhat  into  the  white 
substance  beneath  the  motor  area. 

12.  A  boy,  aged  ten,  much  emaciated  and  anaemic,  was  in  a  state 
of  deepening  coma  when  examined  for  the  first  time.  He  lay  upon 
his  back  picking  alternately  at  the  bedclothes  and  at  his  lips.  The 
pulse  was  130,  small,  feeble,  and  irregular.  Respiration  was  irregu- 
lar (20-30  per  minute).  Temperature,  103^°  Fah.  There  was  con- 
jugate deviation  of  the  eyes  to  the  left.  The  pupils  were  of  moderate 
size,  equal,  and  reacted  to  light.  There  was  some  rigidity  of  the 
muscles  of  the  back  and  sides  of  the  neck.  The  right  arm  and  leg 
and  the  left  arm  were  the  seat  of  rigidity,  which  varied  somewhat 
in  degree  from  hour  to  hour.  No  distinct  loss  of  power  could  be 
made  out.  The  knee-jerk  of  the  right  side  was  exaggerated.  The 
left  knee-jerk  could  not  be  tested  as  the  leg  and  hip-joint  were  immo- 
bilized on  account  of  an  exacerbation  of  the  hip-joint  disease  from 
which  the  patient  had  suffered  several  years.  Examination  revealed 
the  presence  of  a  considerable  grade  of  optic  neuritis. 

The  most  important  localizing  symptoms  in  this  case  were  symp- 
toms of  an  irritative  nature — rigidity  in  the  extremities,  conjugate 
deviation  of  the  eyes  and  rigidity  of  the  muscles  at  the  back  and  sides 
of  the  neck.  The  presence  of  these  conditions  indicated  a  diffuse 
meningeal  process.  The  rigidity  of  the  right  limbs  and  the  conju- 
gate deviation  of  the  eyes  to  the  left  were  referred  to  irritation  of 
different  portions  of  the  left  and  right  motor  regions  respectively. 
The  rigidity  of  the  neck  muscles  was  referred  to  irritation  of  struc- 
tures at  the  base  of  the  brain.  It  was  inferred  from  the  presence  of 
the  irritative  symptoms  just  mentioned,  from  the  presence  of  double 
optic  neuritis  and  the  considerable  elevation  in  temperature,  that  the 
morbid  process  was  inflammatory  ;  in  other  words,  a  meningitis 
affecting  both  the  base  and  convexity  of  the  brain.  The  presence  of 
hip-disease  made  it  exceedingly  probable  that  the  process  was  tuber- 
cular in  nature.  No  physical  signs  of  lung  disease  could  be  detected. 
The  presence  of  optic  neuritis  and  of  irregular  respiration  suggested 
that  the  process  was  tubercular,  although  both  these  conditions  may 
be  and  are  met  with  in  other  forms  of  meningitis. 

The  diagnosis  of  meningitis  was  confirmed  by  the  history  of  the 
case.  The  patient  had  had  hip-disease  for  several  years.  About  ten 
days  before  the  examination  above  recorded  he  had  an  exacerbation 
of  pain  in  the  hip,  with  increase  of  rigidity  of  the  muscles  about  the 


6^2        DISEASES   OF  THE   NERVOUS   SYSTEM. 

joint.  During  this  the  temperature  rose  to  105°  and  he  complained 
of  general  headache.  The  temperature  fell  to  normal  and  the  head- 
ache stopped.  About  this  time  he  vomited  once  without  known 
gastric  cause.  Four  days  before  the  examination  the  temperature 
rose  to  103°  and  the  patient  complained  of  intense  headache.  The 
temperature  continued,  ranging  between  101°  and  104°;  there  was  re- 
peated vomiting,  and  delirium  developed.  Two  days  before,  there  was 
widespread  rigidity  and  temporary  paralysis  of  the  left  arm  and  leg. 

On  the  ninth  day  after  the  examination  the  patient  died.  At  the 
autopsy  was  found  tubercular  meningitis  of  the  base  and  convexity  of 
the  brain.     Fresh  miliary  tubercles  were  present  in  both  lungs. 

13.  A  boy,  aged  twenty,  complained  for  several  months  (probably 
five  or  six)  of  headache  and  of  numbness  and  occasional  "  twitching" 
in  the  right  leg.  In  time  the  right  leg  became  weak  and  occasional 
twitchings  occurred  in  the  right  arm,  the  fingers  of  which  some- 
times became  numb.  When  examined  for  the  first  time  the  patient 
was  in  fair  general  health  but  suffered  from  severe  and  almost  con- 
tinuous headache,  which  was  sometimes  general,  sometimes  limited 
to  the  left  side  of  the  head.  The  right  leg  showed  some  loss  of 
power,  which  was  most  marked  in  the  muscles  below  the  knee. 
There  was  no  wasting  of  the  muscles,  and  the  electrical  reactions 
were  normal.  The  right  knee-jerk  was  exaggerated,  and  an  ankle 
clonus  could  be  obtained  on  this  side.  Tactile  sensibility  was  dimin- 
ished on  the  foot  and  lower  part  of  the  leg.  In  the  arm  there  was 
slight  loss  of  power  in  the  flexors  of  the  wrist  and  fingers,  as  shown 
by  diminution  of  the  grasping  power.  From  time  to  time,  usually 
several  times  a  day,  there  occurred  convulsive  twitchings  in  the  right 
leg.  At  times  these  spasms  were  confined  to  the  anterior  and  poste- 
rior tibial  groups  of  muscles,  at  other  times  they  extended  to  the 
muscles  of  the  right  hand  and  forearm  and,  more  rarely,  to  the  right 
side  of  the  face.  In  some  of  these  seizures  in  which  the  spasm  was 
not  limited  to  the  leg  the  patient  became  unconscious  for  a  few  min- 
utes. There  was  a  temporary  increase  in  weakness  in  the  extremities 
after  they  had  been  the  seat  of  spasm. 

Intellect  was  unimpaired,  but  speech  was  somewhat  disordered. 
There  was  usually  a  decided  slowness  in  speech  and  an  undue  sepa- 
ration of  syllables.  At  times  the  patient  was  unable  to  think  of  the 
names  of  familiar  objects  as  paper,  ink,  knife,  etc.  Spoken  and 
written  words  were  perfectly  understood.  The  use  of  objects  was 
perfectly  understood,  and  the  patient  was  distressed  at  his  inability 


ILLUSTRATIONS   OF   DIAGNOSIS.  673 

to  recall  and  utter  familiar  words.  The  motor  speech  defect  was 
regularly  worse  after  spasm,  whether  this  was  or  was  not  accom- 
panied by  loss  of  consciousness.  At  times  the  motor  speech  defect 
was  very  slight.  Examination  of  the  fundus  of  either  side  showed  a 
high  grade  of  optic  neuritis.  The  temperature,  pulse,  and  respiration 
of  the  patient  were  normal. 

It  was  inferred  from  the  hemiplegic  distribution  of  the  paralysis 
and  spasm,  from  the  disturbance  of  speech,  and  from  the  severity 
of  the  headache,  that  the  patient  was  suffering  from  an  intracranial 
process.  The  initial  involvement  of  the  right  leg,  and  the  gradual 
extension  of  the  symptoms  (weakness  and  spasm)  to  the  right  arm, 
made  it  exceedingly  probable  that  the  lesion  involved  the  left  motor 
tract  where  the  paths  for  the  leg  and  arm  are  farther  separated  than 
in  the  internal  capsule  or  the  parts  below  ;  in  other  words,  that 
the  lesion  involved  the  motor  tract  somewhere  above  the  internal 
capsule — in  the  motor  cortex  or  the  corona  radiata.  From  the 
frequently  repeated  clonic  spasm  it  was  inferred  that  the  lesion 
invaded  the  motor  cortex  or  the  white  substance  immediately  be- 
neath it.  The  extension  of  the  paralysis  and  spasm  made  it  proba- 
ble that  the  morbid  process  began  in  the  motor  structures  related  to 
the  leg  and  had  subsequently  extended  to  the  arm.  It  was  learned 
that  the  involvement  of  the  face  in  spasm  was  a  recent  development, 
and  this  indicated  that  the  morbid  process  was  gradually  invading  the 
path  for  the  face. 

As  to  the  nature  of  the  lesion  there  could  be  little  doubt.  The 
gradual  development  of  the  symptoms  during  a  period  of  several 
months  made  it  certain  that  the  morbid  process  was  either  a  new 
growth  or  an  inflammation.  The  inflammations  which  it  was  neces- 
sary to  consider  were  chronic  meningitis  and  abscess.  Only  a 
chronic  syphilitic  meningitis  could  give  rise  to  well  marked  focal 
symptoms,  and  it  was  doubtful  whether  such  decided  focal  symp- 
toms as  existed  in  this  case  could  be  explained  by  a  purely  menin- 
gitic  process.  No  history  of  syphilis  could,  however,  be  obtained, 
and  while  syphilitic  infection  could  not  be  positively  excluded,  there 
was  reason  to  believe  such  infection  very  unlikely.  An  abscess  occu- 
pying the  subcortical  motor  region  would  account  for  all  the  focal 
symptoms  present,  and  perhaps  for  the  headache.  But  there  were 
no  causal  indications  of  abscess — no  ear  or  bone  disease,  no  evi- 
dences of  suppuration  elsewhere,  not  even  a  history  of  injury  to  the 
head.     Moreover,  the  absence  of  fever  made  abscess  improbable. 


6/4         DISEASES   OF   THE   NERVOUS   SYSTEM. 

On  the  other  hand,  everything  learned  from  the  examination  and 
history  of  the  case  pointed  to  the  presence  of  tumor.  The  gradual 
but  distinct  progress  of  well  marked  focal  symptoms,  especially 
paralysis  and  spasm,  the  severe  and  constant  headache,  the 
presence  of  a  high  grade  of  optic  neuritis,  the  absence  of  fever — 
all  these  conditions  favored  the  diagnosis  of  tumor. 

The  diagnosis  of  the  nature  of  the  tumor  was  difficult ;  could  not, 
in  fact,  be  made.  The  absence  of  a  history  of  syphilis  made  a  syphi- 
loma unlikely.  The  good  general  condition  of  the  patient,  the  ab- 
sence of  fever  during  several  weeks'  observation,  and  the  absence  of 
physical  signs  of  tubercular  lung  disease  made  a  solitary  tubercle  un- 
likely, but  did  not  justify  its  positive  exclusion.  Of  the  remaining 
forms  of  tumors,  glioma  and  sarcoma  were  the  ones  to  be  most  seri- 
ously considered  ;  but  between  these  it  was  impossible  to  decide. 
The  diagnosis  of  cerebral  tumor  was  confirmed  by  autopsy.  During- 
the  remaining  six  weeks  of  the  patient's  life  the  paralysis  extended  to 
the  face  and  tongue,  and  a  high  grade  of  motor  aphasia  was  devel- 
oped. The  number,  intensity,  and  extent  of  the  unilateral  spasms  in- 
creased, and  the  patient  one  day  had  an  apoplectic  seizure,  with  re- 
peated general  convulsions,  in  which  he  died.  The  autopsy  revealed 
a  large  glioma  involving  the  white  matter,  and,  to  a  less  extent,  the 
cortex  of  the  left  hemisphere,  in  the  motor  region,  and  the  adjacent 
portion  of  the  frontal  lobe.  The  tumor  was  highly  vascular.  In  the 
middle  of  the  mass  was  a  recent  hemorrhage  of  considerable  size, 
which  was  undoubtedly  the  direct  cause  of  the  apoplectic  seizure  im- 
mediately preceding  death. 

14.  A  woman,  aged  forty-five,  presented  herself  with  weakness  and 
loss  of  sensation  iu  her  right  arm.  Examination  showed  that  there 
was  some  loss  of  power  in  all  the  muscles  of  the  arm,  but  no 
movements  were  entirely  lost.  There  was  no  wasting  of  the 
limb,  and  all  the  muscles  reacted  normally  to  faradic  and  galvanic 
stimulation.  There  was  loss  of  sensibility  to  pain  and  diminution  in 
tactile  sensibility  over  the  entire  arm  as  high  as  a  sharply  defined  line 
over  the  acromion  to  the  axilla.  There  were  no  trophic  or  vaso- 
motor changes  in  the  limb.  The  knee-jerks  were  active,  but  not 
exaggerated.  The  patient  was  well  nourished  and  in  good  general 
health,  barring  irregular  menstruation  incidental  to  the  climacteric. 

The  presence  of  weakness  in  the  right  arm  without  muscular  atro- 
phy and  changes  in  the  electrical  irritability  of  the  muscles  made  it 
at  once  evident  that  the  monoplegia  was  of  cerebral  origin.   The  seg- 


ILLUSTRATIONS   OF   DIAGNOSIS.  675 

mental  distribution  of  the  motor  and  sensory  loss,  and  the  sharp  limi- 
tation of  the  latter,  made  it  exceedingly  probable  that  these  symptoms 
were  dependent  on  disturbance  of  the  functions  of  the  cortex,  and 
were  due  to  functional  and  not  to  organic  disease.  The  functional 
nature  of  the  disturbance  was  furthermore  indicated  by  the  entire  ab- 
sence of  all  indications  of  organic  cerebral  disease.  Interrogation  of 
the  patient  elicited  the  fact  that  the  arm  trouble  had  developed  a  few 
weeks  before,  within  a  few  minutes  after  the  announcement  of  the 
sudden  death  of  her  brother.  The  dependence  of  the  monoplegia 
upon  emotional  disturbance  left  no  doubt  that  it  was  of  purely  func- 
tional (hysterical)  nature.  Applications  of  the  faradic  current  to  the 
weak  arm  caused  an  immediate  improvement  in  grasping  power  and  in 
tactile  sensibility.  It  gave  rise  also  to  partial  return  of  sensibility  to 
pain  in  irregular  areas  over  the  arm.  These  facts  were  additional 
confirmation  of  the  hysterical  nature  of  the  case. 

15.  A  boy,  aged  ten,  was  picked  up  in  the  street  in  an  unconscious 
condition  and  brought  to  the  hospital.  When  seen  a  few  minutes 
after  he  was  having  irregular  movements  of  nystagmus  and  clonic 
spasms  in  the  lower  extremities.  The  seizures  began  regularly  in  the 
left  leg  and  extended  to  the  right  leg,  recurred  every  few  minutes,  and 
lasted  from  ten  to  sixty  seconds.  The  spasm  involved  chiefly  the  an- 
terior and  posterior  tibial  groups  of  muscles.  The  limbs  were  quite 
relaxed  after  each  paroxysm.  A  convulsive  seizure  could  readily  be 
excited  by  dorsal  flexion  of  the  right  foot,  or  by  an  attempt  to  test  the 
knee-jerk.  On  the  right  side  no  knee-jerk  could  be  obtained  ;  on  the 
left  side  the  knee-jerk  was  exaggerated.  No  true  ankle  clonus  could 
be  obtained,  but  dorsal  flexion  of  the  left  foot  gave  rise  to  irregular 
semi-voluntary  contractions  of  the  calf-muscles,  which  in  a  few  sec- 
onds passed  into  spasm  of  the  same  distribution  as  the  spontaneous 
seizures.  The  patient  could  with  difliculty  be  partially  roused  for  a 
few  seconds.  The  rectal  temperature  was  loof  °,  the  pulse  100,  weak, 
and  irregular. 

In  the  absence  of  any  knowledge  of  the  history  of  this  case  it  was 
impossible  to  come  to  a  final  conclusion  as  to  the  diagnosis.  The 
most  conspicuous  symptom,  clonic  spasm  in  the  lower  extremities,  in- 
dicated the  presence  of  an  irritative  process  in  some  part  of  the  motor 
path.  That  this  irritation  was  of  cerebral  origin  was  rendered  prac- 
tically certain  by  the  presence  of  stupor  and  nystagmus.  The  com- 
bination of  clonic  spasm,  stupor,  and  elevation  of  temperature  might 
have  suggested  meningitis,  but  the  slight  degree  of  the  fever,  the 


676         DISEASES   OF   THE  NERVOUS   SYSTEM. 

rapid  recurrence  of  the  clonic  spasn:is,  the  absence  of  rigidity,  and 
presence  of  nystagmus  would  not  have  lent  much  support  to  this  view. 
The  presence  of  nystagmus  suggested  the  dependence  of  most  of  the 
symptoms  upon  a  general  disturbance  of  cerebral  functions.  No 
diagnosis  was  made,  and  it  was  decided  to  watch  the  further  develop- 
ment of  the  symptoms  before  attempting  to  come  to  a  definite  con- 
clusion. The  next  morning  all  the  symptoms  had  passed  away.  It 
was  learned  that  the  patient  had  slipped  upon  the  sidewalk  and  had 
fallen,  striking  his  head  against  the  stone,  just  before  being  brought 
into  the  hospital.  The  symptoms  that  have  been  described  were 
therefore  due,  in  all  probability,  to  a  severe  concussion  of  the 
brain. 


INDEX 


Abasia,   121 
Abducens  nerve,  54 
Abducens    nerve,     examina- 
tion of,  607 
Abducens  nerve,  paralysis  of, 

496 
Abscess  of  brain,  293,  363 
Abscess  of  spinal  cord,   294, 

441 
Achilles  jerk,  631 
Acoustic  nerve,  65-69 
Acoustic  nerve,  examination 

of,  614 
Action-tremor,  103 
^sthesiometer,  use  of,  638 
Age    as    factor    in    nervous 

disease >  307 
Agraphia,  214 
Alcohol,  abuse  of,  311 
Alcoholic  coma,  206 
Alcoholic  delirium,  596 
Alcoholic  meningitis,  365 
Alcoholic  neuritis,  539-544 
Alcoholism,  acute,  596 
Alexia,  218 
Amaurosis,  159 
Amblyopia,  varieties  of,  159- 

162 
Amnesic  aphasia,  219 
Amyotrophic  lateral  sclerosis, 

470 
iVnsemia  of  brain,  276 
Ansemia  of  spinal  cord,  277 
Anesthesia,  143-148 
Anaesthesia  dolorosa,  441 


Analgesia,  148 
Anarthria,  210 
Aneurism,   intracranial,    278, 

403-406 
Aneurism   of  basilar   artery, 

405 
Aneurism  of  internal  carotid, 

405 

Aneurism  of  middle  cerebral 
artery,  405 

Angiospasm,  277 

Ankle  clonus,  142,  631 

Anosmia,  158 

iVnterior  crural  nerve  paraly- 
sis, 531 

Anterior  fossa  of  skull,  le- 
sions of,   250 

Anterior  horns  of  cord,  le- 
sions of,  254 

Anterior  nerve-roots,  lesions 
of,  267 

Aphasia,  211 

Aphasia,  amnesic,  219 

Aphasia,  ataxic,  214 

Aphasia,  conduction,  219 

Aphasia,  examination  for,  644 

Aphasia,  motor,   212 

Aphasia,  sensory,  212 

Aphonia,  hysterical,  564 

Apoplectic  softening,  379 

Apoplexy,  203 

Apoplexy  without  hemor- 
rhage, 371 

Apraxia,  218 

Arachnoid  membrane,    74 

Aran-Duchenne  type  of  mus- 
cular atrophy,  471 


677 


678      DISEASES    OF    THE    NERVOUS    SYSTEM. 


Argyll-Robinson   pupil,    132, 

458,  627 
Arm-type  of  progressive  mus- 
cular atrophy,  478 
Arsenical  neuritis,  547 
Articulation,   defects  of,   210 
Associated  movements,   118 
Association  fibres,  13 
Association-tracts,  lesions  of, 

236 
Astasia,  121 
Astasia-abasia,  565 
Ataxia,   119 

Ataxia,  determination  of,  624 
Ataxia,  hereditary,  465 
Ataxia  of  tabes  dorsalis,  459 
Ataxic  paraplegia,  472 
Atheroma,      acute      cerebral 

softening  from,  374 
Atheroma  of  cerebral  arteries, 

282 
Athetoid  movements,  115 
Athetoid     movements,   post- 
hemiplegic, 115 
Athetosis,   115 
Athetosis,  primary,  115 
Athetosis,  symptomatic,  117 
Atonic  atrophy,  474 
Atrophy,  muscular,  187,  469 
Atrophy  of  optic  nerve,  173- 

176 
Auditory  nerve,  65 
Auditory  symptoms,  177 
Auditory  tract,  67-69 
Auras,    98 
Aurae,  sensory,  98 
Aurae  of  special  senses,  99 
Aural  vertigo,  181 
Axis-cylinders,  5 


B 


Babinski's  reflex,  631 
Base  of  brain,  lesions  of,  250 
Basilar  artery  aneurism,  405 
Basilar  ineningitis,  356 
Beri-beri,  551 
Biceps  jerk,  627 
Bird-claw  hand,  525 


Birth-palsy,  brachial,  529 
Birth-palsy,  cerebral,  389 
Blood  supply,  loss  of,  85 
Blood   supply   of   brain   and 

cord,  75-80 
Bones     and    joints,     trophic 

changes  in,  185 
Brachial  birth-palsy,  529 
Brachial  neuritis,  528 
Brachial  plexus,  47 
Brain,  10 
Brain,  abscess    of,  363,  394- 

396 
Brain,  anaemia  of,  276 
Brain,  congestion  of,  275 
Brain,  dropsy  of,  422 
Brain,  embolic   softening   of, 

372 
Brain,  inflammation  of,  285 
Brain,  tumor  of,  363 
Broca's  centre,  212 
Brown-Sequard's     paralysis, 

92-93. 
Bulbar  inco-ordination,  123 
Bulbar  paralysis,  416-418 
Burdach,  columns  of,  22 


Cadaveric   position   of  vocal 

cords,  134 
Caisson  paralysis,  441 
Capsular  hemorrhage,  369 
Capsule,  internal,  31 
Capsule,  internal,  lesions  of. 

239 
Carbonic  oxide  neuritis,  548 
Cardiac  disease,  influence  of, 

343 
Caries    .of     vertebrse,     as     a 
cause  of  cord  disease,  427, 

443 
Catalepsy,  113-115 
Cauda  equina,  19 
Cauda  equina,  lesions  of,  268 
Caudate  nuclei.  15 
Causal  indications,  306 
Cell,  nerve,  5 
Central  convolutions,  30 


INDEX. 


679 


"Centres,"  9 

Centrum  ovale,  disease  of,  236 

Centrum    ovale,    hemorrhage 

of,  369 
Cephalic  sensations,   157 
Cerebellar  hemorrhage,   369 
Cerebellar       in  co-ordination, 

121 
Cerebellar  titubation,  121 
Cerebellum,  17 
Cerebellum,  lesions  of,  247 
Cerebral  abscess,  363 
Cerebral,    arteries,    atheroma 

of,  282 
Cerebral  birth-palsy,  389 
Cerebral  commissures,   13 
Cerebral  concussion,  597-599 
Cerebral  cortex,  10 
Cerebral  embolism,  281 
Cerebral     hemorrhage,     203, 

367-371  ^       ., 

Cerebral  paralvsis,   mfantile, 

386  •       ' 

Cerebral  sinuses,  thrombosis 
of,  284 

Cerebral  softening,  acute,  371 
Cerebral   softening,    embolic, 

372 
Charcot  s  joint  disease,  186 
Cheyne-Stokes       respiration, 

202,  224 
Choked  disk,   169 
Chvostek's  reflex,  614 
Chorea,  584-587 
Chorea,  hereditary,  586 
Chorea,  Huntington's,  586 
Chorea,  post-hemiplegic,  118, 

586 
Choreatic  paresis,  118 
Choroiditis,  176 
Chronic  meningitis  in  infants, 

366 
Ciliary  muscle,   paralysis   of, 

496 
Cilio-spinal  centre,  29 
Cilio-spinal  reflex,  626 
Cincture-pain,    153 
Circumflex    ner\'e    paralysis, 

519 


!    Clarke,  column  of,  40 
Claustrum,  lesions  of,  240 
Cleavage  method,  i 
Clitoris  crises,  229 
Clonic  convulsions,  102 
Cochlea,  65 

Cold,  exposure  to,  340 
Columns  of  Goll.  disease  of, 

258 
Coma,  202 
Coma,  alcoholic,  206 
Coma,  diabetic,  206 
Coma,  hysterical,  205 
Coma,  uraemic,   205 
Compression   of  spinal  cord, 

443-445 
Concentric        limitation       of 

visual  field,  162 
Concussion,  cerebral,  597-599 
Conduction  aphasia,  219 
Confluent  articulation,  211 
Congestion  of  brain,  275 
Congestion  of  cord,  276 
Conjugate  deviation,  126 
Conjugate     deviation,    para- 
lytic, 126 
Conjugate     deviation,     spas- 
modic, 126 
Conjunctival  reflex,  626 
Consciousness,  loss  of,  201 
Consciousness,     loss     of,     in 

convulsions,  98 
Contraction,  111-113 
Contracture,  111-113 
Convulsions,  95-103 
Convulsions,  general,  96 
Convulsions,  internal.  102 
Convulsions,     localized,     97, 

O  o  n 

•^^ 
Convulsions,  partial,  97 

Cord,  congestion  of,  276 
Cord,    transverse    lesions    of, 

262 
Cord,  unilateral  lesion  of,  258 
Corneal  reflex.   626 
Corpora  quadrigemina.   15 
Corpora      quadrigemina,     le- 
sions of,  240 
Corpus  callosum,  13 


68o      DISEASES    OF    THE    NERVOUS    SYSTEM. 


Corpus  callosum,   lesions  of, 

237 
Corpus  restifonnis,  65 
Corpus   striatum,   lesions  of, 

238 
Cortical  hemorrhage,  369 
Cortical  inco-ordination,  i2q 
Cramp  of  calf  muscles,  102 
Cranial  nerve-nuclei,    17 
Cranial  nerves,  47 
Cranio-cerebral    topography, 

80 
Cremasteric  reflex,  626 
Crises,  clitoridal,  229 
Crises    of    locomotor    ataxia, 

459 
Crossed  anaesthesia,   244 
Crossed  pyramidal  tract,  34 
Cross-legged  progression,  455 
Crura  cerebri,    15 
Crura  cerebri,  lesions  of,  241 
Crush  of  spinal  cord,  445-448 


D 


Deafness,  nervous,  177 
Defective  central  vision,  161 
Defects  of  articulation,  210 
Defects   of   muscular   power, 

determination  of,   622 
Degeneration,  301 
Degeneration,  reaction  of,  190 
Deglutition  in  bulbar  paraly- 
sis, 417 
Deiter'r,  nucleus,  65 
Delirium,  206 
Delirium,  alcoholic,  596 
Delirium  tremens,  596 
Delusions  of  general  paresis, 

420 
Dementia  paralytica,  419 
Dendrites,  5 
Dermographism,  201 
Deviation  of  eyes,  127 
Diabetes,  345 
Dialectic  coma,  206 
Diabetic  convulsions,  206 
Diabetic  neuritis,  345 


Diagnosis    of    clinical   types, 

352 
Diagnosis  of  nature  of  lesion, 

274 
Diaphragm,  paralysis  of,  516 
Diphtheritic  infection,  322 
Diphtheritic  neuritis,  549 
Diphtheritic  paralysis,  322 
Diplegia,  91 
Diplopia,  128,  610 
Diseases  of  brain,  352 
Diseases  of  peripheral  nerves, 

354 
Diseases    of    special    nerves, 

495 
Diseases  of  spinal  cord,  354, 

426 
Diver's  paralysis,  441 
Double  vision,  128 
Drug-treatment,  influence  on 

nervous  diseases,  346 
Dura,  haematoma  of,  367 
Dura  mater,  74 
Dysarthria,  210 
Dyslexia,   219 
Dystrophies,  muscular,  472 
Dystrophies,  progressive 

muscular,  474 


E 


Electrical  examination,  631- 

637 
Embolic   softening  of  brain, 

372 
Embolism     of     cerebral     ar- 
teries, 281 
Embolism  of  spinal  cord,  441 
Encephalomalacia,   371 
Endarteritis,  syphilitic,  378 
Endolymph,  65 
Epidemic  cerebro-spinal 

meningitis,  357 
Epigastric  reflex,  626 
Epilepsy,  576-582 
Epilepsy,  nocturnal,  577 
Epilepsy,  psychical,  577 
Erb's  paralysis,  529 


INDEX. 


68  I 


Erb's     type     of    progressive 

muscular  dystrophy,   482 
Erroneous  projection,  609 
Erysipelas  and  nervous  affec- 
tions, 326 
Examination  of  the  patient, 

602 
Exhaustion  paralysis,  99 
Exposure  to  cold,  340 
Exposure  to  heat,  341 
External  capsule,  lesions  of, 

240 
External  plantar  nerve,  par- 
alysis of,  532 
External      popliteal      nerve, 

paralysis  of,  532 
Extradural  hemorrhage,  380- 

385 
Eyeball,  trophic  changes  in, 

185 


Facial  nerve,  62 

Facial  i;erve,  examination  of, 

613 
Facial  nerve,  superior  branch 

of,  63,  64 
Facial  paralysis,  502-506 
Facial  paralysis,  double,  505 
Facial  spasm,  506 
False  wryneck,  513 
Festination,   122 
Fibrillation,   106 
Fifth  nerve,  57 
Fifth  nerve,  paralysis  of,  498 
Fissure  of  Rolando,  81 
Fissure  of  Sylvius,  82 
Focal  symptoms,  204 
Foot  clonus,  142,  630 
Foot  phenomenon,  630 
Foramen  of  Monro,  75 
Fortification  spectrum,  167 
Fourth  nerve,  53 
Fourth  nerve  paralysis,  496 
Fragilitas  ossium,  186 
Friedrich's  disease,  349,  465- 

469 
Frontal  lobe,  lesions  of,   234 


Galton's  whistle,  615 

General  paralysis  of  insane, 
419 

General  paresis,  419 

General  paresis,  course  of, 
421 

General  paresis,  delusions  of, 
420 

General  paresis,  differential 
diagnosis  of,  421—422 

General  paresis,  pupillary 
changes  in,  421 

General  paresis,  speech  in, 
420 

General  paresis,  symptoma- 
tology of,  419-421 

General  paresis,  tremor  in, 
420 

Geniculate   ganglion,    63 

Girdle  pain,  153 

Glioma,  298 

Glossopharyngeal    nerve,   69 

Glossopharyngeal  nerve,  ex- 
amination of,  616 

Glossopharyngeal  nerve,  mo- 
tor fibres  of,  69 

Glossopharyngeal  nerve  par- 
alysis, 507 

Glossopharyngeal  nerve,  taste 
fibres  of,  69 

Glossy  skin,  494 

Gluteal  reflex,  626 

Grandmal  epilepsy,  577 

Gray  cord  substance,  lesions 
of,  254 

Gray  tubercle  of  Rolando,  59 

Gudden's  atrophy  method,  2 

Gustatory  symptoms,    183 


H 


Habits,  influence  of,  310 
Haematoma    of    dura    mater, 

367 
Hallucinations,  olfactory,  159 
Headache,  154 


682        DISEASES    OF    THE    NERVOUS    SYSTEM. 


Heat,  exposure  to,  influence 

of,   341 
Hemianaesthesia,  144 
HemiancBSthesia,  crossed,  145 
Hemianesthesia,      hysterical. 

Hemianopsia,  163 
Hemianopsia,    homonymous, 

164 
Hemianopsia,  lateral,  164 
Hemianopsia,  nasal,  164 
Hemianopsia,  temporal,  163 
Hemianoptic   pupillary  inac- 
tion, 133 
Hemiataxia,  120 
Hemichorea,  586 
Hemicrania,  582 
Hemiopia,  163 
Hemiplegia,  89,  204,  232 
Hemiplegia,    "complete,"    86 
Hemiplegia,  crossed,  91-93 
Hemiplegia,  double,  91 
Hemiplegia,  hysterical,  563 
Hemiplegia,   infantile,   392 
Hemiplegia     from    lesion    of 

internal  capsule,  239 
Hemiplegia,  recovery  from, 91 
Hemiplegia,  sensory  disturb- 
ances of,  91 
Hemiplegia,  spinal,  92 
Hemorrhage,  capsular,  369 
Hemorrhage,   cerebellar,   369 
Hemorrhage,cerebral,367-3  7i 
Hemorrhage,  cortical,   369 
Hemorrhage  .extradural,  380- 

385 

Hemorrhage  in  centrum 
ovale,  369 

Hemorrhage,  infantile  menin- 
geal, 367,  380 

Hemorrhage  into  cord,  280 

Hemorrhage  into  cord-mem- 
branes, 280 

Hemorrhage  into  cord-sub- 
stance, 434 

Hemorrhage,        intracrainal, 

277.  367-371 
Hemorrhage,  intraspinal,  432 
Hemorrhage,  meningeal,  277 


Hemorrhage,  meningeal 

spinal,  432-433 
Hemorrhage,  pontal,  369 
Hemorrhage,  retinal,  176 
Hemorrhage,     subarachnoid. 

Hemorrhage,  ventricular,  369 
Hemorrhagic     myelitis,    435, 

438 

Hereditary  ataxia,  465 

Hereditary  chorea,  586 

Heredity,   347 

Huntington's  chorea,  586 

Hydrocephalus,  422 

Hydrocephalus,  diagnosis  of, 
425-426 

Hydrocephalus,  types  of, 
423-425  _ 

Hyperacusis,  616 

Hyperaemia  of  brain,  275 

Hyperassthesia,  151 

Hyperalgesia,  151 

Hyperosmia,  159 

Hypertonicity,  109 

Hypertrophy,  muscular,   190 

Hypertrophy,  pseudo-mus- 
cular, 479-480 

Hypoglossal  nerve,  72 

Hypoglossal  nerve,  exam- 
ination of,  619 

Hypoglossal  nerve  paralysis, 

514 
Hypotonus,  109 
Hysteria,  364,  533-567 
Hysterical  aphonia,  564 
Hysterical  coma,  205 
Hysterical      hemianaesthesia, 

564 
Hysterical  hemiplegia,  563 
Hysterical  monoplegias,  559- 

561 
Hysterical    paraplegia,    561- 

563 
Hysterical  ptosis,  565 
Hysterical  strabismus,   565 


Illustrations     of     diagnosis, 
656-676 


INDEX. 


683 


Incontinence  of  feces,  228 
Incontinence  of  urine,  227 
Inco-ordination,  119 
Inco-ordination,  bulbar,  123 
Inco-ordination,      cerebellar, 

121 
Inco-ordination,  cortical,  120 
Inco-ordination,     peripheric, 

125 
Inco-ordination,  spinal,  123 
Inequality  of  pupils,  133 
Infantile    cerebral   paralysis , 

386 
Infantile  hemiplegia,  392 
Infantile      meningeal      hem- 
orrhage, 367,  380,  389 
Infantile  paralysis,  449 
Infectious  diseases,  influence 

of,   315 
Inflammation  of  bram,  285 
Inflammation    of   nerve -sub- 
stance, 86 
Influenza  and  nervous  affec- 
tions, 327 
Inhibition,  irritative,  86 
"Intellectual  tract,"    19 
Intention  tremor,  103 
Intercellular  substance,  5 
Internal  capsule,  hemorrhage 

into,  367-369 
Internal  capsule,  lesions  of, 

239 

Internal  carotid  aneurism, 
405 

Internal  popliteal  nerve  par- 
alysis, 532 

Intracranial  abscess,  363 

Intracranial  aneurism,  278, 
403-406 

Intracranial         hemorrhage, 

367-371 

Intracranial  tumor,  397-403 

Iris,  paralysis  of,  496 

Irritability  of  nerve,  dimin- 
ished, 198 

Irritability  of  nerve,  in- 
creased, 199 

Irritation  of  optic  apparatus,- 
167 


Island  of  Reil,  lesions  of, 
236 

J 

Jacksonian  epilepsy,   98 
Jaw-jerk,  627 

Juvenile  type,  progressive 
dystrophy,  482 

K 

Kidney  disease,  influence  on 
nervous  system,  344 

Knee-jerk,  628 

Knee-jerk,  loss  of,  138,  458 

Knee-jerks,  exaggeration  of 
(in  general  paresis),  421 

L 

Landouzy-Dejerine  type  of 
progressive  muscular  dys- 
trophy, 483 

Landry's  paralysis,  553-556 

Laryngeal  nerves,  71 

Laryngeal   symptoms,    134 

Laryngismus  stridulus,  136 

Larynx,  adductor  paralysis 
of,  136 

Larynx,  total  abductor  par- 
alysis of,  135 

Larynx,  total  bilateral  par- 
alysis of,  134 

Larynx,  total  unilateral  par- 
alysis of,  134 

Larynx,  unilateral  abductor, 
paralysis  of,  135 

Lead  neuritis,  545-547 

Lead-poisoning,  329 

"Leg-type,"  progressive  mus- 
cular atrophy,  477 

Lemniscus,  41 

Lenticular  nucleus,  15 

Leprosy,  anaesthetic,  552 

Leprous  neuritis,  552 

Leptomeningitis,   286 

Light  action  of  pupil,  627 

Light  inaction  of  pupil,  627 

Lightning  pains  of  locomotor 
ataxia,  457 

Localization,  rules  of,  230 


684       DISEASES   OF    THE    NERVOUS    SYSTEM. 


Locomotoir  ataxia,  457-462 
Locomotor      ataxia,      ataxic 

phenomena  of,  458 
Locomotor  ataxia,   crises  of, 

459 

Locomotor  ataxia,  differ- 
ential diagnosis  of,  460-461 

Locomotor  ataxia,  lightning 
pains  of,  457 

Locomotor  ataxia,  neuralgic 
stage  of,  459 

Locomotor  ataxia,  pre-ataxia 
stage  of,  458 

Lumbar  enlargement,  21 

Lumbar  plexus,  47 

Lumbar    plexus,    lesions    of, 

533 
Lumbar  puncture,  360 


M 


Malingering,  599-601 

Masturbation,  314 

Measles  and  nervous  affec- 
tions, 325 

Mechanical  injury  of  nerve- 
substance,  85 

Median-nerve   paralysis,    522 

Median-ulnar  nerve  paralysis, 

527 
Medulla  oblongata,  lesions  of, 

246 

Meningeal  hemorrhage,  379- 

384 
Meningeal    hemorrhage,     m- 

fantile,  379-384,  389 
Meninges  of  brain  and  cord, 

74 
Meningitis,  286 
Meningitis,     acute     internal, 

428 
Meningitis,  alcoholic,  365 
Meningitis,  basilar,  356 
Meningitis,  cerebral,  355-360 
Meningitis,        cerebro-spinal, 

357 
Meningitis,  chronic,   365 
Meningitis, chronic,  in  infants, 

366 


Meningitis,  chronic  internal, 

430  .       , 

Meningitis,   diseases  simulat- 
ing, 361-367 
Meningitis,  external,  291 
Meningitis,  internal,  291,  428 
Meningitis  of  convexity,  356 
Meningitis,  purulent,  287,  356 
Meningitis,  simple,  287,  359 
Meningitis,  spinal,  290,  426 
Meningitis,     syphilitic,     289, 

319,  366 
Meningitis,    tubercular,    288, 

316,  358 
Mental  deterioration,  simple, 

208 
Mental  shock,  343 
Mental  symptoms,  201 
Mercurial  poisoning,  332 
Middle  cerebral  artery  aneur- 
ism, 405 
Middle  fossa  of  skull,  disease 

in,  251 
Middle   peduncle   of  cerebel- 
lum, lesions  of,  249 
Migraine,  582-584 
Migraine,  ophthalmic,  583 
Mind-blindness,  217 
Mind-deafness,  218 
Mixed  nerve,  37 
Mobile  spasm,  115 
Monoplegia,  hysterical,   559- 

561 
Monoplegias,  89,  94,  232 
Monospasm,  101 
Moral  sense,  defects  of,   209 
Morbid  blood-states,  345 
Morvan's  disease,  492 
Motor  oculi,  examination  of, 

607 
Motor  paralysis,  87 
Motor  points,  190 
Motor  tract,  29 
Multiple  neuritis,  538 
Multiple  sclerosis,  41 1-4 16 
Muscle  pain  sense,  643 
Muscles,  excessive  use  of,  341 
Muscles,  trophic  changes  in, 
187 


INDEX. 


685 


Muscular  atrophy,  187,  469 
Muscular    atrophy,    progres- 
sive, 472 
Muscular  dystrophies,  472 
Muscular  hypertrophy,  190 
Muscular  sense,  643 
Muscular  sensibility,  loss  of, 

150 

Muscular  tenderness,  154 

Musculocutaneous  nerve  par- 
alysis, 519 

Musculospiral  nerve  paraly- 
sis, 520 

Myelitis,  acute,  435-440 

Myelitis,  chronic,  442 

Myelitis,  diffuse,  438 

Myelitis,  hemorrhagic,  435, 
438 

Myelitis,  transverse,  436,  438 

Myelitis,  types  of,  435-436 


N 


Nasal  hemianopsia,   164 
Nerve-elements,   wasting   of, 

86 
Nerve-substance,     inflamma- 
tion of,  86 
Nerve-substance,  mechanical 

injury  of,  85 
Nerves,  tumors  of,  300 
Nervous  deafness,  177 
Neuralgia,  590-594 
Neuralgic  stage  of  tabes  dor- 

salis,  458 
Neuralgiform  pains,  592-594 
Neurasthenia,  575-576 
Neuritis,  292,  493-495 
Neuritis,  alcoholic,  539-544 
Neuritis,  carbonic  oxide,  548 
Neuritis,   diphtheritic,   549 
Neuritis,  disseminated,  538 
Neuritis,  leprous,   552 
Neuritis,  migrans,  494 
Neuritis,  multiple,  538 
Neuritis,  optic,   169 
Neuritis,    primary    brachial, 

528 
Neuritis,  rheumatic,  498 


Neuritis,  tuberculous,  316 

Neurons,  3 

Neuroses  of  occupation,  594- 

596 
Neuroses,  traumatic,  567 
Nocturnal  epilepsy,   581 
Nuclear        ophthalmoplegia, 

409 
Nucleus  ambiguus,  71 
Nucleus  angularis,   67 
Nucleus  tecti,   67 
Nystagmus,   129 


O 


Obstetrical  paralysis,  529 
Obturator    nerve     paralysis, 

530. 
Occipital  lobe,  lesions  of,  235 
Occupation     neuroses,     594- 

596 
Ocular  muscles,  paralysis  of, 

495 
Ocular  nerves,  56 

Ocular    paralyses,  types    of, 

497-498 
Ocular  vertigo,   182 
Oculomotor  paralysis,   495 
Olfactory  hallucinations,  159 
Olfactory  nerve,  48 
Olfactory  nerve,  examination 

of,    604 
Olfactory  symptoms,  158 
Ophthalmic  migraine,  583 
Ophthalmoplegia,       nuclear, 

406-411 
Ophthalmoplegia,  periodical, 

411 
Ophthalmoplegia,    recurrent, 

411 
Ophthalmoscopic       changes, 

168 
Optic     apparatus,     irritation 

of,    167 
Optic  nerve,  49 
Optic  nerve,  atrophy  of,  173 
Optic  nerve,  examination  of, 

Optic  neuritis,  169 


686       DISEASES    OF    THE    NERVOUS    SYSTEM. 


Optic  thalamus,   15 

Optic    thalamus,    lesions   of, 

238 
Optic  tra^ct,  50 
Over-fatigue,  341 


Pachymeningitis  interna 

hemorrhagica,   367 
Pachymeningitis,  spinal,  427 
Pain,   152 

Pain,  neuralgiform,    592-594 
Pain  referred  to  spine  153 
Pain,  reflected,  592 
Pain,  sensibility  to,  639 
Papillitis,  170 
Para-anaesthesia,  146 
Paracentral  lobule,  30 
Paraesthesiae,    152 
Paralysis,    acute  anaesthetic, 

553-556 
Paralysis  agitans,  588-590 
Paralysis,  bulbar,  416-418 
Paralysis,    determination   of, 

623 
Paralysis,  infantile,    448 
Paralysis    of   ciliary    muscle, 

496 
Paralysis  of  sphincter  iridis, 

496 
Paraplegia,  93 
Paraplegia,  ataxic,  462 
Paraplegia,    hysterical,    458, 

561-563 
Paraplegia,  primary  spastic, 

454-457 

Paraplegia,   spastic,   453 

Paresis,  95 

Paresis,  general,  419 

Parietal  lobe,  lesions  of,  234 

Parkinson's  disease,  587 

Pars  accessorius  of  vagus,  ex- 
amination of,  616 

Patellar  reflex,  130 

Patellar  reflex,  loss  of,  138 

Patheticus,  53 

Patheticus,  examination  of, 
607 


Patient,  examination  of,  602 
Periodical    ophthalmoplegia, 

411 
Peripheral  nerves,  lesions  of, 

273 
Peripheral  nerves,  tumors  of, 

534 
Peroneal  form  of  progressive 

muscular  atrophy,  477 
Peroneal     nerve      paralysis, 

532 
Petit  mal  epilepsy,  577 
Pharyngeal  nerves  and  plex- 
us, 70,  71 
Pharyngeal  paralysis,  508 
Pharyngeal  spasm,  508 
Phrenic  nerve  paralysis,  520 
Pia  mater,  75 

Plantar  nerve  paralyses,   532 
Plantar  reflex,  626 
Pneumogastric  nerve,  70 
Pneumogastric  nerve  paraly- 
sis, 507 
Pneumonia  and  nervous  af- 
fections, 326 
Poliomyelitis,  448 
Poliomyelitis,  acute  anterior, 

449 
Poliomyelitis,    chronic,    452, 

472 
Poliomyelitis,  subacute,  452 
Polyneuritis,  538 
Pons  Varolii,  lesions  of,  242 
Pontal  hemorrhage,  369 
Position   of  morbid   process, 

350 

Post-epileptic  stupor,  205 

Posterior  fossa  of  skull,  dis- 
ease in,  251 

Posterior  horn  of  cord,  dis- 
ease of,  255 

Posterior  nerve-roots,  lesions 
of,  268 

Posterior  thoracic  nerve  par- 
alysis, 517 

Postero-extemal  column  of 
cord,  disease  of,  257 

Post-hemiplegic  a  t  h  e  t  o  i  d 
movements,   115 


INDEX. 


687 


Post-hemiplegic  chorea,  118, 
586 

Postero-internal  column  of 
cord,  disease  of,  258 

Pre-ataxic  stage  of  tabes  dor- 
salis,  458 

Precuneus,  30 

Pregnancy,  346 

Pressure  lesions,  85 

Progressive  muscular  atro- 
phy, 472-477 

Projection  fibres,  13 

Propulsion,  122 

Pseudo-hypertrophic  paraly- 
sis, 479 

Pseudo-muscular      hypertro- 

pV.  479 
Pseudo-paralytic     (terminal) 

stage  of  ataxia,  459 
Pseudo  tabes,  541 
Psychical  epilepsy,  577 
Psychoneurosis,      traumatic, 

568-574 
Ptosis,  130,  496 
Ptosis,  hysterical,  565 
Pulse,  222 
P  upil,  Argyll- Robertson  ,132, 

627 
Pupil,  contraction  of,  132 
Pupil,  dilatation  of,  131 
Pupil,     dilatation     of,     with 

immobility,  132 
Pupil,  light  action  of,  627 
Pupil,  light  inaction  of,   657 
Pupillary       accommodation, 

loss  of,  496 
Pupillary  changes  in  general 

paresis,  421 
Pupillary    inaction,    hemian- 

opic,  133 
Pupillary    reaction    to    light, 

loss  of,  496 
Pupillary  reflex,  626 
Pupillary  symptoms,  131 
Pupils,  inequality  of,  133 
Purulent  meningitis,  356 

R 

Rachialgia,  153 


Reaction  of  degeneration,  190 
Reflected  pains,  592 
Reflex  action,  abnormal,  2)1 
Reflex  action,  excess  of,   140 
Reflex  action,  loss  of,  137 
Reflex  arc,  43 
Reflex,  Babinski's,  631 
Reflex  centre,  43 
Reflex,  Chvostek's,  614 
Reflex,  cilio-spinal,  626 
Reflex,  conjunctival,  626 
Reflex,  corneal,  626 
Reflex,  epigastric,  626 
Reflex,  gluteal,  626 
Reflex  influences,  339 
Reflex,  patellar,  130 
Reflex  paths,  43 
Reflex,  plantar,,  626 
Reflex,  pupillary,  626 
Reflexes,  deep,  44 
Reflexes,      examination      of, 

625-631 
Respiration,  223 
Respiration,    Cheyne-Stokes, 

202 
Retinal  hemorrhages,  176 
Retinitis,  albuminuric,  176 
Retropulsion,  123 
Retrocollic  spasm,  513 
Rheumatic  neuritis,  498 
Rheumatism      (acute)      and 

nervous  affections,  326 
Rickets,  345 
Rigidity,   1 08-1 11 
Rigidity,  tonic,    102 
Rolandic  region,  30 
Romberg  symptom,  408 


Sacral  plexus,  47 
Scanning  speech,  211 
Sciatic  nerve  paralysis,  531 
Sciatica,   593 

Sclerosis,  disseminated,  416 
Sclerosis,  insular,  416 
Secondary  degeneration,  2 
Secondary  deviation,  608 
Semicircular  canals,  65 


688       DISEASES    OF    THE    NERVOUS    SYSTEM. 


Senile  tremor,  589 
Sense,  muscle-pain,  643 
Sense,  muscular,  643 
Sense,  temperature,  640 
Sensibility  to  pain,  639 
Sensibility  to  touch,  637 
Sensory  examination,    637 
Sensory     paralyses    of    fifth 

nerve,  498-499 
Sensory  symptoms,  143 
Sensory  tract,  38 
Serratus    magnus    paralysis, 

517 
Sex,  309 

Sexual  excess,  313 
Sexual    functions,     disorders 

of,  228 
"Shaking  palsy,"  587 
"Sick  headache,"  582 
Sieveking'sassthesiometer,638 
Silver  poisoning,   7,7,7, 
Sinus-thrombosis,  384 
Skin,  trophic  changes  in,  184 
Small  sciatic  nerve  paralysis, 

533 
Small-pox  and  nervous  aiiec- 

tions,  325 
Softening  of  brain,  281 
Solitary  tubercle,  316 
Soul-blindness,  217 
Spasm,  determination  of,  624 
Spasmodic  wryneck,  512 
Speech  disturbances,  209 
Speech  in  general  paresis,  420 
Sphincters,  affections  of,  226 
Spinal  accessory  nerve,  71 
Spinal   accessory   nerve,    ex- 
amination of,  618 
Spinal   accessory  nerve    par- 
alysis,  509 
Spinal  cord,  19 
Spinal  cord,  abscess  of,  441 
Spinal  cord,  anaemia  of,  277 
Spinal  cord,  compression  of, 

443-445 
Spinal  cord,  crush  of ,  445-448 
Spinal  cord,  degeneration  dis- 
eases of,  453 
Spinal  cord,  diseases  of,  426 


Spinal  cord,  embolism  of,  441 
Spinal  cord,  hemorrhage  into, 

280 
Spinal    cord,    localization    of 

lesions  in,  253 
Spinal-cord  topography,  80 
Spinal  inco-ordination,  123 
Spinal  meningitis,  426 
Spinal  nerves,  44 
Spinal     paralysis,     atrophic, 

255 
Spinal  paralyses,  spastic,  257 
Spinal  topography,  80 
Sterno-mastoid  paralysis,  510 
Stilling's  column,  40 
Strabismus,  127 
Strabismus,  convergent,    128 
Strabismus,  divergent,  128 
Strabismus,  external,  128 
Strabismus,  hysterical,  565 
Strabismus,  internal,  128 
Stupor,   202 

Stupor,  post-epileptic,  205 
Subarachnoid       hemorrhage, 

383 

Subarachnoid  space,  74 

Subcortical  lesions,  237 

Subdural  space,  74 

Superior  gluteal  nerve  par- 
alysis,  531 

Superior  parietal  lobule,  30 

Supinator  jeik,  627 

Supra-scapular  nerve  par- 
alysis, 518 

Sylvian  fissure,  82 

Sylvian  line,  81 

Sympathetic  nervous  system, 
26 

Symptomatology  of  nervous 
diseases,   84 

Symptoms,  onset  of,  305 

Syphilis  as  a  factor  in  degen- 
erative diseases,  320 

Syphilitic  endarteritis,  318 

Svphi'litic  endarteritis  and 
hemorrhage,  378 

Syphilitic  infection,  318 

Syphilitic  meningitis,  366 

Syphilitic  thrombosis,  373 


INDEX. 


689 


Syringomyelia,  488-493, 
System-diseases  of  cord,  254 


Tabes  dorsalis,  457 

Tache  cerebrale,  201 

Temperature,  221 

Temperature  sense,  640 

Temperature  sense,  loss  of, 
149 

Temporal  lobe,  lesions  of,  235 

Tetanoid  spasms,  loi 

Tetanus,  338 

Thomsen's  disease,  349 

Thrombosis  of  cerebral  ar- 
teries, 281 

Thrombosis  of  c  e  re  b  r  a  1 
sinuses,  284 

Thrombosis  of  sinus,  primary, 

384 

Thrombosis  of  sinus,  secon- 
dary, 386 

Thrombosis,   simple   arterial, 

375 
Tic  convulsif,  506 
Tinnitus  aurium,  179 
Titubation,  cerebellar,  121 
Tobacco,    excessive    use    of, 

Tongue,  paralysis  of,  514 

Tongue,  spasm  of,  515 

Tonic  atrophy,  474 

Tonic  spasms,  loi 

Torticollis,  511 

Touch,  sensibility  to,  637 

Transverse    lesion    of     cord, 

262 
Trapezius  paralysis,  509 
Trauma   and  nervous    affec- 
tions, 334 
Traumatic  hysteria,  567 
Traumatic  neurosis,  567 
Traumatic       psychoneurosis, 

568-574 
Tremor,  103-106 
Tremor,  action,  103 
Tremors,     determination  of, 
624 


Tremor,  intention,  103 
Tremor,  senile,  104,  589 
Tremor,  simple,  104 
Triceps  jerk,  627 
Trifacial  nerve,  57 
Trifacial  nerve,  examination 

of,  611 
Trophic  symptoms,  183 
Trousseau's  symptom,  loi 
Tubercles  of  choroid,  176 
Tubercle,  solitary,  316 
Tubercular  meningitis,  358 
Tuberculosis  of  vertebrae,  317 
Tuberculous  infection,  316 
Tumor,      intracranial,      295, 

397-403 
Tumor,  intraspinal,   485-488 
Tumor  of  brain,  7,63 
Tumor  of  nerves,  300 
Tumors  of  peripheral  nerves, 

534 
Tumors  of  spinal  cord,  298 
Typhoid   fever   and  nervous 

affections,  323 


U 


Ulnar  nerve  paralysis,  524 

Unilateral  lesions  of  cord,  258 

Urcemic  coma,  205 

Urine,  226 

Urine,  incontinence  of,  227 


V 


Vagus,  examination  of,  616- 

618 
Vagus  nerve,  70 
Vascular  disease,  344 
Vasomotor  symptoms,  199 
Ventricular  hemorrhage,  369 
Vertigo,  180 
Vertigo,  aural,  181 
Vertigo,  essential,  180 
Vertigo,  gastric,  182 
Vertigo,  ocular,  182 
Vestibule,   65 
Vision,  defective  central,  161 


-i- 


MEDICAL  PUBLICATIONS. 


Vertebrate  Embryology.  By  A.  Milnes  Marshall,  M.D., 
Professor  of  Zoology  in  Owens  College,  England,  and  C. 
H.  Hurst,  Demonstrator  of  Zoology  in  Owens  College. 
Fully  illustrated,  8vo $6  oo 

Medical  and  Surgical  Nursing.  A  Treatise  on  Modern  Nursing 
from  the  Physician's  and  Surgeon's  Standpoint,  for  the 
Guidance  of  Graduate  and  Student  Nurses,  together  with 
Practical  Instruction  in  the  Art  of  Cooking  for  the  Sick. 
By  H.  J.  O'Brien,  M.D.      i2mo,  net  .  .     $i   50 

The  Pathology  of  the  Eye.  By  J.  Herbert  Parsons, 
B.S.D.Sc.  (Lond.),  F.R.C.S.  (Eng.),  Assistant  Ophthal- 
mic Surgeon,  University  College  Hospital.  In  4  parts. 
Fully  illustrated.     Sold  separately.     Each,  net  .     $3   50 

Vol.      I. — Histology.      Part  I. 

Vol.    II.—         "  Part  II. 

Vol.  III. — Pathology.     Part  I. 

Vol.   IV.^         "  Part  II. 

A  Junior  Course  in  Practical  ZoOlogy.  By  A.  Milnes  Mar- 
shall, M.D.,  Professor  of  Zoology  in  Owens  College, 
England,  and  C.  H.  Hurst,  Demonstrator  of  Zoology  in 
Owens  College,  England.  With  48  woodcuts.  Third 
edition,  revised.     Cloth,  Svo       ,  .  .     $3   50 

The  Story  of  the  Bacteria  and  their  Relations  to  Health  and 
Disease.  By  T.  Mitchell  Prudden,  M.D.  i6mo, 
cloth $0  75 

Dust  and  its  Dangers.  Illustrated.  By  T.  Mitchell  Prud- 
den.     i6mo,  cloth      .  .  .  .  .  .     $0  75 

Drinking-Water  and  Ice  Supplies,  and  their  Relation  to  Health 
and  Disease.  By  T.  M.  Prudden,  M.D.  Illustrated, $0  75. 

An  Introduction  to  Vertebrate  Embryology.  Based  on  the 
Study  of  the  Frog  and  the  Chick.  By  Albert  Moore 
Reese,  Ph.D.  (Johns  Hopkins),  Associate  Professor  of 
Histology  and  Embryology  in  Syracuse  University. 
With  84  illustrations.      i2mo,  net      .         .         .     $1   40 

Bacteria.  Especially  as  they  are  related  to  the  economy  of 
nature,  to  industrial  processes,  and  to  the  public  health. 
By  George  Newman,  M.D.,  F.R.S.  (Edinburgh),  D.P.H. 
(Camb.),  etc.,  Demonstrator  of  Bacteriology  in  King's 
College,  London.  With  24  micro-photographs  of  actual 
organisms  and  over  70  other  illustrations.      8vo       $2   00 

Hygienic  Measures  in  Relation  to  Infectious  Diseases.  In- 
formation as  to  the  Cause  and  Mode  of  Spreading  of 
Certain  Diseases;  the  Preventive  Measures  that  should 
be  resorted  to;  Isolation,  Disinfection,  etc.  By 
George  F.  H.  Nuttall,  M.D.,  Ph.D.  (Gottingen.) 
i6mo,  cloth  .  .  .  .  .  .  .     $0   75 


MEDICAL  PUBLICATIONS. 


Diagnosis  of  Organic  Nervous  Diseases.  By  Christian  A, 
Herter,  M.D.,  Professor  of  Pharmacology  and  Thera- 
peutics at  Columbia  University.  Revised  by  L.  Pierce 
Clark,  M.D.,  Consulting  Neurologist  at  the  Manhattan 
State  Hospital,  With  about  loo  illustrations.  Crown 
8vo,  cloth  .  .  $3   oo 

The  Mental  Functions  of  the  Brain.  An  Investigation  into 
their  Localization  and  their  Manifestation  in  Health  and 
Disease.  By  Bernard  Hollander,  M.D.  (Freiburg 
I.B.),  M.R.C.S.,  L.R.C.P.  (London).  Illustrated  with 
the  Clinical  Records  of  Eight  Hundred  Cases  of  Localized 
Brain  Derangements  and  with  several  Plates.  8vo. 
(By  mail,  $3.75) Net,  $3   50 

Hysteria,  Brain  Tumor,  and  other  Nervous  Affections.  A 
Series  of  Essays.    By  Mary  Putnam  Jacobi,  M.D.  $2   00 

The  Question  of  Rest  for  Women  during  Menstruation.  Being 
the  Boylston  Prize  Essay  of  Harvard  University  for 
1876.  By  Mary  Putnam  Jacobi,  M.D.,  Professor  of 
Materia  Medica  in  the  Women's  Medical  College,  N.  Y. 
With  Sphygmographic  Tracings  Showing  the  Variations 
in  Arterial  Tension,  and  Tables  Giving  Results  of  250 
Urea  Analyses  of  Urine.  Third  edition.  8vo,  cloth, 
illustrated  .  .  .  .  .  .  .     $2   00 

Infant  Diet.  By  A.  Jacobi,  M.D.,  Clinical  Professor  of  Dis- 
eases of  Children,  College  of  Physicians  and  Surgeons, 
New  York.  Revised,  enlarged,  and  adapted  for  popular 
use  by  Mary  Putnam  Jacobi,  M.D.    i2mo,  boards,  $0  50 

Mental  State  of  Hystericals.    By  Pierre  Janet,  Litt.D.,  M.D., 
Professor  of  Philosophy  at  the  College  Rollin.     With  a 
Preface  by  Prof.  J.  M.  Charcot.     Translated  by  Caro- 
line Rollin  Corson.   8vo.   (By  mail,  $3.75.)   Net,  $3   50 
Part  I.  Mental  Stigmata,    Part  II,  Mental  Accidents. 

Short  Talks  with  Young  Mothers  on  the  Management  of 
Infants  and  Young  Children.  By  Charles  Gilmore 
Kerley,  M.D.,  Lecturer  on  Diseases  of  Children,  N.  Y. 
Polyclinic  Medical  School  and  Hospital;  Assistant  At- 
tending Physician,  Babies'  Hospital,  New  York;  Phy- 
sician Out-Patient  Department  Babies'  Hospital,  New 
York,     1 2mo,  illustrated.     (By  mail,  $1.35.)     Net,  $1   25 

A  Text-Book  for  Training  Schools  for  Nurses.  By  P.  M. 
Wise,  M.D.,  President  of  the  New  York  State  Commis- 
sion of  Lunacy.  With  an  Introduction  by  Edward 
CowLES,  M.D.,  Physician-in-Chief  and  Superintendent 
McLean  Hospital,  Boston,  Mass.  Two  volumes.  i6mo, 
illustrated.     Sold  separately.     Each  .  .  .$125 

Comparative  Physiology  of  the  Brain  and  Comparative  Psy- 
chology. With  Special  Reference  to  the  Invertebrates. 
By  Jacques  Loeb,  M.D.,  Professor  of  Physiology  in  the 
University  of  Chicago.     Illustrated,     8vo.         .     $1   75 


MEDICAL  PUBLICATIONS. 


Heredity  and  Human  Progress.  By  W.  Duncan  McKim, 
M.D.      8vo,  cloth,  net  .  .  .  .  .     $i    50 

Diagnosis,  Differential  Diagnosis,  and  Treatment  of  Diseases 
of  the  Eye.  By  A.  E.  Adams,  M.D.,  Instructor  in  Dis- 
eases of  the  Eye  in  the  Post-Graduate  Medical  College; 
Assistant  Surgeon  to  Manhattan -Eye  and  Ear  Hospital. 
New  York,  etc.      i6mo,  cloth      .  .  .  .     $1   00 

Suggestive  Therapeutics.  A  Treatise  on  the  Nature  and 
Uses  of  Hypnotism.  By  H.  Bernheim,  M.D.,  Professor 
in  the  Faculty  of  Medicine  at  Nancy.  Translated  from 
the  second  and  revised  French  edition  by  Christian  A. 
Herter,  M.D.,  of  New  York.     8vo,  cloth  .  $3   50 

The  Liver  of  Dyspeptics,  and  particularly  the  Cirrhosis  pro- 
duced by  Auto-Intoxication  of  Gastro-Intestinal  Origin. 
(Clinical  Anatomo-Pathological,  Pathogenic,  and  Ex- 
perimental Study.)  By  Dr.  Emile  Boix,  Paris,  France. 
Authorized  translation  by  Paul  Richard  Brown,  M.D., 
U.  S.  Army.      Illustrated,  8vo,  cloth  .  .     $2   00 

The  Student's  Manual  of  Diseases  of  the  Skin.  With  Analysis 
of  Twenty  Thousand  Consecutive  Cases  and  a  Formulary. 
Fourth    edition.     By    L.    D.    Bulkley,    M.D.       Large 

i6mo  .  .  .  .  .  .  .  .  .$125 

Acne  and  its  Treatment.  A  Practical  Treatise  Based  on  the 
Study  of  One  Thousand  Five  Himdred  Cases  of  Diseases 
of  the  Sebaceous  Glands.  By  L  D.  Bulkley,  M.D. 
8vo,  illustrated  ,  .  .  .  .  .  .     $2   00 

Eczema.  With  an  Analysis  of  Eight  Thousand  Cases  of  the 
Disease.  By  L.  D.  Bulkley,  M.D.  i2mo.  Third  edi- 
tion   Net,  $1   25 

A  Text-Book  of  Materia  Medica  for  Nurses.  By  Lavinia  L. 
Dock,  Graduate  of  Bellevue  Training  School  for  Nurses, 
Late  Superintendent  of  Nurses,  Illinois  Training  School 
for  Nurses,  etc.  Fourth  edition,  revised  and  enlarged  to 
conform  with  the  U.  S.  Pharmacopoeia  of  1900.      i2mo. 

Net,  $1    50 

Infection  and  Immunity;  or,  The  Causes  and  Prevention  of 
Infectious  Diseases.  By  George  M.  Sternberg,  M.D., 
LL.D.,  Surgeon-General  U.  S.  Army  (Retired).  8vo, 
illustrated.      (By  mail,  $1.90)  .  .  .         Net,  $1    75 

The  Care  of  the  Consumptive.  A  Consideration  of  the 
Scientific  Use  of  Natural  Therapeutic  Agencies  in  the 
Prevention  and  Cure  of  Consumption;  together  with  a 
Chapter  on  Colorado  as  a  Resort  for  Invalids.  By 
Charles  Fox  Gardiner,  M.D.,  Member  of  the  American 
Climatological  Association.     Cloth      .  .  .     $1    25 


New  York  G.  P.  PUTNAM'S  SONS  London 


RG348  H44 

1907 

Herter 


